Stima dei decessi attribuibili all'inquinamento da NO2, PM10 e PM2,5 nella Città di Milano nel 2019.

BACKGROUND: there is growing evidence that exposure to environmental pollutants affects health, including mortality, chronic diseases, and acute diseases. The World Health Organisation has recently revised downwards the safety thresholds for exposure to environmental pollutants. The City of Milan (CoM) has particularly high levels of pollution; this is due both to the presence of various emission sources and to climatic and orographic conditions. OBJECTIVES: to describe the health effects of exposure to pollutants, measured by deaths due to environmental exposure to NO2, PM10, and PM2.5 in 2019. DESIGN: observational study. Using a pollutant concentration estimation model, annual mean values of NO2, PM10, and PM2.5 were estimated for the CoM in 2019. The number of deaths attributable to each exposure was estimated using risk functions available in the literature; the values recommended by the new World Health Organisation guidelines were used as counterfactual exposure limits. SETTING AND PARTICIPANTS: the population assisted by the Agency for Health Protection of Milan and resident in the CoM on 01.01.2019, aged 30 years or older. The place of residence was georeferenced and the population was followed up until 31.12.2019. Deaths and their causes were obtained from the Causes of Death Registry. MAIN OUTCOME MEASURES: deaths attributable to exposure from non-accidental causes, cardiovascular diseases, respiratory diseases, and lung cancer were estimated. RESULTS: in 2019, the estimated annual average level of NO2 was 36.6 µg/m3, that of PM10 was 24.9 µg/m3, and that of PM2.5 was 22.4 µg/m3, with levels varying across the city area. Concerning exposure to NO2, in 2019 10% of deaths for natural causes were estimated to be attributable to annual mean levels of NO2 above 10 µg/m3. As regard PM2.5, 13% of deaths for natural causes and 18% of deaths from lung cancer were attributable to an annual mean level above 5 µg/m3. The impact of exposure to particulate matter on mortality does not seem to be the same in all the areas of the CoM. CONCLUSIONS: the health impact of exposure to airborne particulate matter in the CoM population is high. It is important that citizens, policy-makers, and stakeholders address this issue, because of its impact on both health and healthcare costs.

Investigation analysis of the acute asthma risk factor and phenotype based on relational analysis with outdoor air pollutants in Xi'an, China.

Asthma is a common chronic heterogeneous disease. Outdoor air pollutants are an important cause of acute asthma. Until now, the association between the risk of acute asthma and outdoor air pollutants is unclear. And the relationship between the different phenotypes of asthma and outdoor air pollutants has not been reported. Thus, an analysis of the association between outdoor air pollutants and daily acute asthma inpatient and outpatient visits in Xi'an, China, from January 1 to December 31, 2018, was conducted. A total of 3395 people were included in the study. The statistical analysis and relational analysis based on the logistic regression were used for illustrating the relatedness of the acute asthma risk factor and phenotype with outdoor air pollutants, while the age, gender, pollen peak and non-pollen peak periods, high type 2 (T2) asthma and non-high T2 asthma were also stratified. Results showed that particulate matter with particle size below 10 µm and 2.5 µm (PM10 and PM2.5), sulfur dioxide(SO2), nitrogen dioxide(NO2), and carbon monoxide(CO) increase the risk of acute asthma and that air pollutants have a lagged effect on asthma patients. PM10, NO2, CO, and Ozone (O3) are associated with an increased risk of acute attacks of high T2 asthma. PM10, PM2.5, SO2, NO2 and CO are associated with an increased risk of acute asthma in males of 0-16 years old. PM10 and PM2.5 are more harmful to asthma patients with abnormal lung function.

Air pollutants, genetic susceptibility, and the risk of incident gastrointestinal diseases: A large prospective cohort study.

A comprehensive overview of the associations between air pollution and the risk of gastrointestinal (GI) diseases has been lacking. We aimed to examine the relationships of long-term exposure to ambient particulate matter (PM) with aerodynamic diameter ≤2.5 µm (PM2.5), 2.5-10 µm (PMcoarse), ≤10 µm (PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOx), with the risk of incident GI diseases, and to explore the interplay between air pollution and genetic susceptibility. A total of 465,703 participants free of GI diseases in the UK Biobank were included at baseline. Land use regression models were employed to calculate the residential air pollutants concentrations. Cox proportional hazard models were used to evaluate the associations of air pollutants with the risk of GI diseases. The dose-response relationships of air pollutants with the risk of GI diseases were evaluated by restricted cubic spline curves. We found that long-term exposure to ambient air pollutants was positively associated with the risk of peptic ulcer (PM2.5 : Q4 vs. Q1: hazard ratio (HR) 1.272, 95% confidence interval (CI) 1.179-1.372, NO2: 1.220, 1.131-1.316, and NOx: 1.277, 1.184-1.376) and chronic gastritis (PM2.5: 1.454, 1.309-1.616, PM10 : 1.232, 1.112-1.366, NO2: 1.456, 1.311-1.617, and NOx: 1.419, 1.280-1.574) after Bonferroni correction. Participants with high genetic risk and high air pollution exposure had the highest risk of peptic ulcer, compared to those with low genetic risk and low air pollution exposure (PM2.5: HR 1.558, 95%CI 1.384-1.754, NO2: 1.762, 1.395-2.227, and NOx: 1.575, 1.403-1.769). However, no significant additive or multiplicative interaction between air pollution and genetic risk was found. In conclusion, long-term exposure to ambient air pollutants was associated with increased risk of peptic ulcer and chronic gastritis.

The impact of short-term exposures to ambient NO2, O3, and their combined oxidative potential on daily mortality.

It is widely recognized that air pollution exerts substantial detrimental effects in human health and the economy. The potential for harm is closely linked to the concentrations of pollutants like nitrogen dioxide (NO2) and ozone (O3), as well as their collective oxidative potential (OX). Yet, due to the challenges of directly monitoring OX as an independent factor and the influences of different substances' varying ability to contain or convey OX, uncertainties persist regarding its actual impact. To provide further evidence to the association between short-term exposures to NO2, O3, and OX and mortality, this study conducted multi-county time-series analyses with over-dispersed generalized additive models and random-effects meta-analyses to estimate the mortality data from 2014 to 2020 in Jiangsu, China. The findings reveal that short-term exposures to these pollutants are linked to increased risks of all-cause, cardiovascular, and respiratory mortality, where NO2 demonstrates 2.11% (95% confidence interval: 1.79%, 2.42%), 2.28% (1.91%, 2.66%), and 2.91% (2.13%, 3.69%) respectively per every 10 ppb increase in concentration, and the effect of O3 is 1.11% (0.98%, 1.24%), 1.39% (1.19%, 1.59%), and 1.82% (1.39%, 2.26%), and OX is 1.77% (1.58%, 1.97%), 2.19% (1.90%, 2.48%), and 2.90% (2.29%, 3.52%). Notably, women and individuals aged over 75 years exhibit higher susceptibility to these pollutants, with NO2 showing a greater impact, especially during the warm seasons. The elevated mortality rates associated with NO2, O3, and OX underscore the significance of addressing air pollution as a pressing public health issue, especially in controlling NO2 and O3 together. Further research is needed to explore the underlying mechanisms and possible influential factors of these effects.

Association between short-term air pollution exposure and perturbation in thyrotropin levels in 1.38 million Chinese women: A national longitudinal analysis, 2014-2019.

Prevalence of subclinical hypothyroidism substantially increased during the last decade in China, which has been commonly/clinically diagnosed as elevation in thyrotropin (thyroid-stimulating hormone [TSH]). Tobacco smoke containing toxic substances has been linked to thyroid dysfunction; however, data on perturbation of TSH following air pollution exposure in human has not been assessed at nationwide population level. We investigated the longitudinal impact of daily ambient air pollution estimated at residential level on serum TSH in 1.38 million women from China's 29 mainland provinces between 2014 and 2019. We observed that particulate matter with aerodynamic diameter ≤ 10 and ≤ 2.5 µm (PM10, PM2.5) and nitrogen dioxide (NO2) at cumulative lag 0-7 days of exposure were associated with percent elevations in TSH (0.88% [95% CI: 0.71, 1.05] per [interquartile range, IQR: 54.8 µg/m3] of PM10; 0.89% [95% CI, 0.71, 1.07] per IQR [40.3 µg/m3] of PM2.5; 2.01% [95% CI: 1.81, 2.22] per IQR [27.4 µg/m3] of NO2). Greater associations were observed in participants living in areas with ≥adequate iodine intake and those with low BMI levels and high inflammation status. Our results suggest that increased concentrations of recent ambient air pollutants at exposure ranges commonly encountered in Asia were associated with increases in TSH, supporting disturbing role of short-term air pollution exposure on the regulation of thyroid hormone homeostasis.

Disentangling impacts of multiple pollutants on acute cardiovascular events in New York city: A case-crossover analysis.

BACKGROUND: Ambient air pollution contributes to an estimated 6.67 million deaths annually, and has been linked to cardiovascular disease (CVD), the leading cause of death. Short-term increases in air pollution have been associated with increased risk of CVD event, though relatively few studies have directly compared effects of multiple pollutants using fine-scale spatio-temporal data, thoroughly adjusting for co-pollutants and temperature, in an exhaustive citywide hospitals dataset, towards identifying key pollution sources within the urban environment to most reduce, and reduce disparities in, the leading cause of death worldwide. OBJECTIVES: We aimed to examine multiple pollutants against multiple CVD diagnoses, across lag days, in models adjusted for co-pollutants and meteorology, and inherently adjusted by design for non-time-varying individual and aggregate-level covariates, using fine-scale space-time exposure estimates, in an exhaustive dataset of emergency department visits and hospitalizations across an entire city, thereby capturing the full population-at-risk. METHODS: We used conditional logistic regression in a case-crossover design - inherently controlling for all confounders not varying within case month - to examine associations between spatio-temporal nitrogen dioxide (NO2), fine particulate matter (PM2.5), sulfur dioxide (SO2), and ozone (O3) in New York City, 2005-2011, on individual risk of acute CVD event (n = 837,523), by sub-diagnosis [ischemic heart disease (IHD), heart failure (HF), stroke, ischemic stroke, acute myocardial infarction]. RESULTS: We found significant same-day associations between NO2 and risk of overall CVD, IHD, and HF - and between PM2.5 and overall CVD or HF event risk - robust to all adjustments and multiple comparisons. Results were comparable by sex and race - though median age at CVD was 10 years younger for Black New Yorkers than White New Yorkers. Associations for NO2 were comparable for adults younger or older than 69 years, though PM2.5 associations were stronger among older adults. DISCUSSION: Our results indicate immediate, robust effects of combustion-related pollution on CVD risk, by sub-diagnosis. Though acute impacts differed minimally by age, sex, or race, the much younger age-at-event for Black New Yorkers calls attention to cumulative social susceptibility.

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

BACKGROUND: Although 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. METHODS: Analyses 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. RESULTS: GDM 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). CONCLUSION: PM2.5 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.

Prenatal exposure to air pollution and BWGA Z-score: Modifying effects of placenta leukocyte telomere length and infant sex.

BACKGROUND: Air pollutants, such as fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3), have been associated with adverse birth outcomes, including low birth weight, often exhibiting sex-specific effects. However, the modifying effect of placental telomere length (TL), reflecting cumulative lifetime oxidative stress in mothers, remains unexplored. METHOD: Using data from a Northeastern U.S. birth cohort (n = 306), we employed linear regression and weighted quantile sum models to assess trimester-average air pollution exposures and birth weight for gestational age (BWGA) z-scores. Placental TL, categorized by median split, was considered as an effect modifier. Interactions among air pollutants, placental TL, infant sex, and BWGA z-score were evaluated. RESULTS: Without placental TL as a modifier, only 1st trimester O3 was significantly associated with BWGA z-scores (coefficient: 0.33, 95% CI: 0.03, 0.63). In models considering TL interactions, a significant modifying effect was observed between 3rd trimester NO2 and BWGA z-scores (interaction p-value = 0.02). Specifically, a one interquartile range (1-IQR) increase in 3rd trimester NO2 was linked to a 0.28 (95% CI: 0.06, 0.52) change in BWGA z-score among shorter placental TL group, with no significant association among longer TL group. Among male infants, there were significant associations between 3rd trimester PM2.5 exposure and BWGA z-scores in the longer TL group (coefficient: -0.34, 95% CI: -0.61, -0.02), and between 1st trimester O3 exposure and BWGA z-scores among males in the shorter TL group (coefficient: 0.59, 95% CI: 0.06, 1.08). For females, only a negative association in 2nd trimester mixture model was observed within the longer TL group (coefficient: -0.10, 95% CI: -0.21, -0.01). CONCLUSION: These findings highlight the need to consider the complex interactions among prenatal air pollutant exposures, placental TL, and fetal sex to better elucidate those at greatest risk for adverse birth outcomes.

Ambient air pollution and rate of spontaneous abortion.

Spontaneous abortion (SAB), defined as a pregnancy loss before 20 weeks of gestation, affects up to 30% of conceptions, yet few modifiable risk factors have been identified. We estimated the effect of ambient air pollution exposure on SAB incidence in Pregnancy Study Online (PRESTO), a preconception cohort study of North American couples who were trying to conceive. Participants completed questionnaires at baseline, every 8 weeks during preconception follow-up, and in early and late pregnancy. We analyzed data on 4643 United States (U.S.) participants and 851 Canadian participants who enrolled during 2013-2019 and conceived during 12 months of follow-up. We used country-specific national spatiotemporal models to estimate concentrations of particulate matter <2.5 µm (PM2.5), nitrogen dioxide (NO2), and ozone (O3) during the preconception and prenatal periods at each participant's residential address. On follow-up and pregnancy questionnaires, participants reported information on pregnancy status, including SAB incidence and timing. We fit Cox proportional hazards regression models with gestational weeks as the time scale to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association of time-varying prenatal concentrations of PM2.5, NO2, and O3 with rate of SAB, adjusting for individual- and neighborhood-level factors. Nineteen percent of pregnancies ended in SAB. Greater PM2.5 concentrations were associated with a higher incidence of SAB in Canada, but not in the U.S. (HRs for a 5 µg/m3 increase = 1.29, 95% CI: 0.99, 1.68 and 0.94, 95% CI: 0.83, 1.08, respectively). NO2 and O3 concentrations were not appreciably associated with SAB incidence. Results did not vary substantially by gestational weeks or season at risk. In summary, we found little evidence for an effect of residential ambient PM2.5, NO2, and O3 concentrations on SAB incidence in the U.S., but a moderate positive association of PM2.5 with SAB incidence in Canada.

Migraine and air pollution: A systematic review.

OBJECTIVE: To systematically synthesize evidence from a broad range of studies on the association between air pollution and migraine. BACKGROUND: Air pollution is a ubiquitous exposure that may trigger migraine attacks. There has been no systematic review of this possible association. METHODS: We searched for empirical studies assessing outdoor air pollution and any quantified migraine outcomes. We included short- and long-term studies with quantified air pollution exposures. We excluded studies of indoor air pollution, perfume, or tobacco smoke. We assessed the risk of bias with the World Health Organization's bias assessment instrument for air quality guidelines. RESULTS: The final review included 12 studies with over 4,000,000 participants. Designs included case-crossover, case-control, time series, and non-randomized pre-post intervention. Outcomes included migraine-related diagnoses, diary records, medical visits, and prescriptions. Rather than pooling the wide variety of exposures and outcomes into a meta-analysis, we tabulated the results. Point estimates above 1.00 reflected associations of increased risk. In single-pollutant models, the percent of point estimates above 1.00 were carbon monoxide 5/5 (100%), nitrogen dioxide 10/13 (78%), ozone 7/8 (88%), PM2.5 13/15 (87%), PM10 2/2 (100%), black carbon 0/1 (0%), methane 4/6 (75%), sulfur dioxide 3/5 (60%), industrial toxic waste 1/1 (100%), and proximity to oil and gas wells 6/13 (46%). In two-pollutant models, 16/17 (94%) of associations with nitrogen dioxide were above 1.00; however, more than 75% of the confidence intervals included the null value. Most studies had low to moderate risks of bias. Where differences were observed, stronger quality articles generally reported weaker associations. CONCLUSIONS: Balancing the generally strong methodologies with the small number of studies, point estimates were mainly above 1.00 for associations of carbon monoxide, nitrogen dioxide, ozone, and particulate matter with migraine. These results were most consistent for nitrogen dioxide.

Multiple myeloma risk in relation to long-term air pollution exposure - A pooled analysis of four European cohorts.

BACKGROUND: Air pollution is a growing concern worldwide, with significant impacts on human health. Multiple myeloma is a type of blood cancer with increasing incidence. Studies have linked air pollution exposure to various types of cancer, including leukemia and lymphoma, however, the relationship with multiple myeloma incidence has not been extensively investigated. METHODS: We pooled four European cohorts (N = 234,803) and assessed the association between residential exposure to nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone (O3) and multiple myeloma. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. RESULTS: During 4,415,817 person-years of follow-up (average 18.8 years), we observed 404 cases of multiple myeloma. The results of the fully adjusted linear analyses showed hazard ratios (95% confidence interval) of 0.99 (0.84, 1.16) per 10 µg/m³ NO2, 1.04 (0.82, 1.33) per 5 µg/m³ PM2.5, 0.99 (0.84, 1.18) per 0.5 10-5 m-1 BCE, and 1.11 (0.87, 1.41) per 10 µg/m³ O3. CONCLUSIONS: We did not observe an association between long-term ambient air pollution exposure and incidence of multiple myeloma.

Acute and subchronic exposure to urban atmospheric pollutants aggravate acute respiratory failure in infants.

Urban air pollution is a major factor that affects the respiratory health of children and adolescents. Less studied is exposure during the first two years of life. This study analyzed the influence of acute and subchronic exposure to urban air pollutants on the severity of acute respiratory failure (ARF) in the first two years of life. This population-based study included 7364 infants hospitalized with ARF. Acute exposure was considered to have occurred 1, 3 and 7 days before hospitalization and subchronic exposure was considered the mean of the last 30 and 60 days. We found that for acute exposure, significant increases in days of hospitalization (LOS) occurred at lag 1 day for NO2 (0.24), SO2 (6.64), and CO (1.86); lag 3 days for PM10 (0.30), PM2.5 (0.37), SO2 (10.8), and CO (0.71); and lag 7 days for NO2 (0.16), SO2 (5.07) and CO (0.87). Increases in the risk of death occurred at lag 1 day for NO2 (1.06), SO2 (3.64), and CO (1.28); and lag 3 days for NO2 (1.04), SO2 (2.04), and CO (1.19). Subchronic exposures at 30 and 60 days occurred for SO2 (9.18, 3.77) and CO (6.53, 2.97), respectively. The associations were more pronounced with higher temperatures and lower relative humidity levels. We concluded that acute and subchronic exposure to higher atmospheric concentrations of all the pollutants studied were associated with greater severity of ARF. The greatest increases in LOS and risk of death occurred with hot and dry weather.

Criteria air pollutants and diabetes mortality classified by different subtypes and complications: A nationwide, case-crossover study.

The associations between air pollution and diabetes mortality of different subtypes and complications were largely unclear. We performed an individual-level, time-stratified case-crossover study among over 0.9 million diabetes deaths from all administrative regions of Chinese mainland during 2013-2019. Daily concentrations of fine particles (PM2.5), coarse particles (PM2.5-10), nitrogen dioxide (NO2) and ozone (O3) were obtained for each decedent using high-resolution prediction models. Conditional logistic regression models were utilized to analyze the data. Each interquartile range increment in PM2.5, PM2.5-10, NO2 and O3 concentrations on lag 0-2 d increased the risks of overall diabetes mortality by 2.81 %, 1.92 %, 3.96 % and 2.15 %, respectively. Type 2 diabetes had stronger associations with air pollution than type 1 diabetes. Air pollutants were associated with diabetic ketoacidosis and diabetic nephropathy, but not other complications. The exposure-response curves were approximately linear with a plateau at higher concentrations of PM2.5, PM2.5-10, and NO2, while the associations for O3 appear to be statistically significant beyond 60 µg/m3. This nationwide study reinforces the evidence of higher risks of acute diabetic events following short-term air pollution exposure. We identified differential effects of air pollutants on various subtypes and complications of diabetes, which require further mechanistic investigations.

Sperm quality decline associated with gaseous pollutant exposure: Evidence from a large cohort multicenter study.

BACKGROUND: Poor sperm quality is a prevalent cause of male infertility, and the association between gaseous ambient air pollutants exposure and semen quality remains unclear. OBJECTIVES: To examine the relationship between gaseous air pollution exposure with semen quality in a large-scale and multi-center study. METHODS: We analyzed 78,952 samples corresponding to 33,234 study subjects from 2014 to 2020. The high-resolution grid pollution dataset was used to estimate personal exposures to CO, SO2, NO2 and O3 across entire stage of semen formation and three crucial stages. The linear mixed models were performed to evaluate the relationships. RESULTS: The results showed that sperm count was inversely related to SO2 exposure (-0.0070, -0.0128 to -0.0011). Decreased sperm concentration was associated with SO2 (-0.0083, -0.0142 to -0.0024), NO2 (-0.0162, -0.0320 to -0.0005) and O3 (-0.0306, -0.0480 to -0.0133) during 0-90 lag days, respectively. Additionally, we observed significant decline of PR and total motility with SO2 exposure. Similar trends were observed for SO2 and CO exposure during 3 key periods. CONCLUSIONS: Our findings suggest that exposure to gaseous air pollutants may have negative impacts on sperm quality. These findings highlight the importance that critical periods of sperm development should be considered when implementing protective measures.

Various ambient air pollutants, residential green spaces, fibrosis 4 scores, genetic susceptibility, and risk of severe liver disease.

BACKGROUND: The relationship of air pollutants and residential exposure to greenspace with severe liver disease remains inconclusive. OBJECTIVE: Our objective was to assess the relationship of joint exposure to air pollutants, residential exposure to greenspaces with new-onset severe liver disease. METHODS: We included 427,697 participants without prior liver diseases from UK Biobank. A weighted air pollution score was calculated based on PM2.5, PM10, PM2.5-10, NO2, and NOX. The percentage of land coverage by residential greenspaces was estimated using land use data. The primary outcome was new-onset severe liver disease, defined as a composite outcome including hospitalization or death due to compensated or decompensated liver cirrhosis, liver failure, and hepatocellular carcinoma. RESULTS: During a median follow-up of 12.0 years, 4572 participants developed severe liver disease. A higher air pollution score was significantly associated with an increased risk of new-onset severe liver disease (per SD increment; adjusted hazard ratio [HR],1.07; 95% confidence interval [CI],1.04-1.10). Moreover, residential greenspace coverage was inversely associated with new-onset severe liver disease (per SD increment; adjusted HR, 0.95; 95% CI,0.92-0.98). Genetic risks of liver cirrhosis did not significantly modify the associations (both P-interactions >0.05). However, we observed a stronger positive association between air pollution scores and new-onset severe liver disease in individuals with higher fibrosis-4 (FIB-4) scores, lower residential greenspaces, hypertension, and smokers (all P-interactions <0.05). Similarly, a more pronounced inverse association between residential exposure to greenspaces and new-onset severe liver disease was found in smokers and individuals with higher FIB-4 scores (both P-interactions<0.05). CONCLUSIONS: Our findings suggest a positive association between air pollution scores and the risk of new-onset severe liver disease, while residential greenspaces show an inverse association. These results underscore the importance of maintaining high exposure to green space and reducing air pollution to prevent serious liver disease.

Effect of NO2 exposure on airway inflammation and oxidative stress in asthmatic mice.

Nitrogen dioxide (NO2) is a widespread air pollutant. Epidemiological evidence indicates that NO2 is associated with an increase of incidence rate and mortality of asthma, but its mechanism is still unclear. In this study, we exposed mice to NO2 (5 ppm, 4 h per day for 30 days) intermittently to investigate the development and potential toxicological mechanisms of allergic asthma. We randomly assigned 60 male Balb/c mice to four groups: saline control, ovalbumin (OVA) sensitization, NO2 alone, and OVA+NO2 groups. The involved mechanisms were found from the perspective of airway inflammation and oxidative stress. The results showed that NO2 exposure could aggravate lung inflammation in asthmatic mice, and airway remodeling was characterized by significant thickening of the airway wall and infiltration of inflammatory cells. Moreover, NO2 would aggravate the airway hyperresponsiveness (AHR), which is characterized by significantly elevated inspiratory resistance (Ri) and expiratory resistance (Re), as well as decreased dynamic lung compliance (Cldyn). In addition, NO2 exposure promoted pro-inflammatory cytokines (IL-6 and TNF-α) and serum immunoglobulin (IgE) production. The imbalance of Th1/Th2 cell differentiation (IL-4 increased, IFN-γ reduced, IL-4/IFN-γ significantly increased) played a key role in the inflammatory response of asthma under NO2 exposure. In a nutshell, NO2 exposure could promote allergic airway inflammation and increase asthma susceptibility. The levels of ROS and MDA among asthmatic mice exposed to NO2 increased significantly, while GSH levels sharply decreased. These findings may provide better toxicological evidence for the mechanisms of allergic asthma risk due to NO2 exposure.

Mortality attributable to ambient fine particulate matter and nitrogen dioxide in Switzerland in 2019: Use of two-pollutant effect estimates.

INTRODUCTION: Air pollution health risk assessments have traditionally used single-pollutant effect estimates for one proxy ambient air pollutant such as PM2.5. Two-pollutant effect estimates, i.e. adjusted for another correlated pollutant, theoretically enable the aggregation of pollutant-specific health effects minimizing double-counting. Our study aimed at estimating the adult mortality in Switzerland in 2019 attributable to PM2.5 from a single-pollutant effect estimate and to the sum of PM2.5 and NO2 from two-pollutant estimates; comparing the results with those from alternative global, European and Swiss effect estimates. METHODS: For the single-pollutant approach, we used a PM2.5 summary estimate of European cohorts from the project ELAPSE, recommended by the European Respiratory Society and International Society for Environmental Epidemiology (ERS-ISEE). To derive the two-pollutant effect estimates, we applied ELAPSE-based conversion factors to ERS-ISEE PM2.5 and NO2 single-pollutant effect estimates. Additionally, we used World Health Organization 2021 Air Quality Guidelines as counterfactual scenario, exposure model data from 2019 and Swiss lifetables. RESULTS: The single-pollutant effect estimate for PM2.5 (1.118 [1.060; 1.179] per 10 µg/m3) resulted in 2240 deaths (21,593 years of life lost). Using our derived two-pollutant effect estimates (1.023 [1.012; 1.035] per 10 µg/m3 PM2.5 adjusted for NO2 and 1.040 [1.023; 1.058] per 10 µg/m3 NO2 adjusted for PM2.5), we found 1977 deaths (19,071 years of life lost) attributable to PM2.5 and NO2 together (23% from PM2.5). Deaths using alternative effect estimates ranged from 1042 to 5059. DISCUSSION: Estimated premature mortality attributable to PM2.5 alone was higher than to both PM2.5 and NO2 combined. Furthermore, the proportion of deaths from PM2.5 was lower than from NO2 in the two-pollutant approach. These seemingly paradoxical results, also found in some alternative estimates, are due to statistical imprecisions of underlying correction methods. Therefore, using two-pollutant effect estimates can lead to interpretation challenges in terms of causality.

Air quality health index (AQHI) based on multiple air pollutants and mortality risks in Taiwan: Construction and validation.

The currently used air quality index (AQI) is not able to capture the additive effects of air pollution on health risks and reflect non-threshold concentration-response relationships, which has been criticized. We proposed the air quality health index (AQHI) based on daily air pollution-mortality associations, and compared its validity in predicting daily mortality and morbidity risks with the existing AQI. We examined the excess risk (ER) of daily elderly (≥65-year-old) mortality associated with 6 air pollutants (PM2.5, PM10, SO2, CO, NO2, and O3) in 72 townships across Taiwan from 2006 to 2014 by performing a time-series analysis using a Poisson regression model. Random effect meta-analysis was used to pool the township-specified ER for each air pollutant in the overall and seasonal scenarios. The integrated ERs for mortality were calculated and used to construct the AQHI. The association of the AQHI with daily mortality and morbidity were compared by calculating the percentage change per interquartile range (IQR) increase in the indices. The magnitude of the ER on the concentration-response curve was used to evaluate the performance of the AQHI and AQI, regarding specific health outcomes. Sensitivity analysis was conducted using coefficients from the single- and two-pollutant models. The coefficients of PM2.5, NO2, SO2, and O3 associated with mortality were included to form the overall and season-specific AQHI. An IQR increase in the overall AQHI at lag 0 was associated with 1.90%, 2.96%, and 2.68% increases in mortality, asthma, and respiratory outpatient visits, respectively. The AQHI had higher ERs for mortality and morbidity on the validity examinations than the current AQI. The AQHI, which captures the combined effects of air pollution, can serve as a health risk communication tool to the public.

Long-term exposure to air pollution and severe COVID-19 in Catalonia: a population-based cohort study.

The association between long-term exposure to ambient air pollutants and severe COVID-19 is uncertain. We followed 4,660,502 adults from the general population in 2020 in Catalonia, Spain. Cox proportional models were fit to evaluate the association between annual averages of PM2.5, NO2, BC, and O3 at each participant's residential address and severe COVID-19. Higher exposure to PM2.5, NO2, and BC was associated with an increased risk of COVID-19 hospitalization, ICU admission, death, and hospital length of stay. An increase of 3.2 µg/m3 of PM2.5 was associated with a 19% (95% CI, 16-21) increase in hospitalizations. An increase of 16.1 µg/m3 of NO2 was associated with a 42% (95% CI, 30-55) increase in ICU admissions. An increase of 0.7 µg/m3 of BC was associated with a 6% (95% CI, 0-13) increase in deaths. O3 was positively associated with severe outcomes when adjusted by NO2. Our study contributes robust evidence that long-term exposure to air pollutants is associated with severe COVID-19.

Disparities in ambient nitrogen dioxide pollution in the United States.

Average ambient concentrations of nitrogen dioxide (NO2), an important air pollutant, have declined in the United States since the enactment of the Clean Air Act. Despite evidence that NO2 disproportionately affects racial/ethnic minority groups, it remains unclear what drives the exposure disparities and how they have changed over time. Here, we provide evidence by integrating high-resolution (1 km × 1 km) ground-level NO2 estimates, sociodemographic information, and source-specific emission intensity and location for 217,740 block groups across the contiguous United States from 2000 to 2016. We show that racial/ethnic minorities are disproportionately exposed to higher levels of NO2 pollution compared with Whites across the United States and within major metropolitan areas. These inequities persisted over time and have worsened in many cases, despite a significant decrease in the national average NO2 concentration over the 17-y study period. Overall, traffic contributes the largest fraction of NO2 disparity. Contributions of other emission sources to exposure disparities vary by location. Our analyses offer insights into policies aimed at reducing air pollution exposure disparities among races/ethnicities and locations.