OBJECTIVE: Disposable face masks are a primary protective measure against the adverse health effects of exposure to infectious and toxic aerosols such as airborne viruses and particulate air pollutants. While the fit of high efficiency respirators is regulated in occupational settings, relatively little is known about the fitted filtration efficiencies of ear loop style face masks worn by the public.
METHODS: We measured the variation in fitted filtration efficiency (FFE) of four commonly worn disposable face masks, in a cohort of healthy adult participants (N = 100, 50% female, 50% male, average age = 32.3 ± 9.2 years, average BMI = 25.5 ± 3.4) using the U.S. Occupational Safety and Health Administration Quantitative Fit Test, for an N95 (respirator), KN95, surgical, and KF94 masks. The latter three ear loop style masks were additionally tested in a clip-modified condition, tightened using a plastic clip to centrally fasten loops in the back of the head.
RESULTS: The findings show that sex is a major determinant of the FFE of KN95, surgical, and KF94 masks. On average, males had an 11% higher FFE relative to females, at baseline testing. We show that a simple modification using an ear loop clip, results in improvements in the average FFE for females but provides comparatively minor changes for males. On average, females had a 20% increased FFE when a clip was worn behind the head, relative to a 6% increase for males.
CONCLUSIONS: The efficacy of a disposable face mask as protection against air contaminants depends on the efficiency of the mask materials and how well it fits the wearer. We report that the sex of the wearer is a major determinant of the baseline fitted filtration efficiency (FFE) of commonly available ear loop style face masks. In addition, we show that a simple fit modifier, an ear loop clip fastened behind the head, substantially improves baseline FFE for females but produces only minor changes for males. These findings have significant public health implications for the use of face masks as a protective intervention against inhalational exposure to airborne contaminants.

To evaluate the modification of allergic dermatitis on the association between PM exposure and allergic rhinitis in preschool children. This cross-sectional study was based on a questionnaire conducted between June 2019 and June 2020 to caregivers of children aged 3 to 6 years in the kindergartens of 7 Chinese cities to collect information on allergic rhinitis and allergic dermatitis. A mature machine learning-based space-time extremely randomized trees model was applied to estimate early-life, prenatal, and first-year exposure of PM1, PM2.5 and PM10 at 1 km×1 km resolution. A combination of multilevel logistic regression and restricted cubic spline functions was used to quantitatively assess whether allergic dermatitis modifies the associations between size-specific PM exposure and the risk of childhood allergic rhinitis. The results showed that out of 28 408 children, 14 803 (52.1%) were boys and 13 605 (47.9%) were girls; the age of children ranged from 3.1 to 6.8 years, with a mean age of (4.9±0.9) years, of which 3 586 (12.6%) were diagnosed with allergic rhinitis. Among all children, 17 832 (62.8%) were breastfed for more than 6 months and 769 (2.7%) had parental history of atopy. A total of 21 548 children (75.9%) had a mother with an educational level of university or above and 7 338 (29.6%) had passive household cigarette smoke exposure. The adjusted ORs for childhood allergic rhinitis among the children with allergic dermatitis as per interquartile range (IQR) increase in early-life PM1(9.8 μg/m3), PM2.5 (14.9 μg/m3) and PM10 (37.7 μg/m3) were significantly higher than the corresponding ORs among the children without allergic dermatitis [OR: 1.45, 95%CI (1.26, 1.66) vs. 1.33, 95%CI (1.20, 1.47), for PM1; OR: 1.38, 95%CI (1.23, 1.56) vs. 1.32, 95%CI (1.21, 1.45), for PM2.5; OR: 1.56, 95%CI (1.31, 1.86) vs. 1.46, 95%CI (1.28, 1.67), for PM10]. The interactions between allergic dermatitis and size-specific PM exposure on childhood allergic rhinitis were statistically significant (Z value=19.4, all P for interaction<0.001). The similar patterns were observed for both prenatal and first-year size-specific PM exposure and the results of the dose-response relationship were consistent with those of the logistic regression. In conclusion, allergic dermatitis, as an important part of the allergic disease progression, may modify the association between ambient PM exposure and the risk of childhood allergic rhinitis. Children with allergic dermatitis should pay more attention to minimize outdoor air pollutants exposure to prevent the further progression of allergic diseases.
本研究评估特应性皮炎在颗粒物暴露与学龄前儿童过敏性鼻炎发生风险关联中的效应修饰作用。采用横断面研究的设计，通过问卷调查的方式于2019年6月至2020年6月在中国7个城市的幼儿园收集了共计28 408名3~6岁学龄前儿童有关过敏性鼻炎和特应性皮炎的信息。运用一种成熟的基于机器学习的时空模型以1 km的空间分辨率水平估算不同城市儿童生命早期、孕期和出生后第1年PM1、PM2.5和PM10暴露水平。采用多水平logistic回归和暴露反应关系相结合的方法定量评估特应性皮炎作为效应修饰因子是否会改变不同粒径颗粒物暴露与儿童过敏性鼻炎发生风险的关联。结果显示，在28 408名儿童中，男孩为14 803名（52.1%），女孩为13 605名（47.9%）；年龄范围是3.1~6.8岁、（4.9±0.9）岁，其中患过敏性鼻炎的儿童为3 586名（12.6%）。在总人群中，母乳喂养持续时间大于6个月的儿童为17 832名（62.8%），父母有过敏史的为769名（2.7%）。母亲教育水平为大学及以上的儿童为21 548名（75.9%）。有被动吸烟暴露的儿童为7 338名（29.6%）。生命早期PM1（9.8 μg/m3）、PM2.5（14.9 μg/m3）和PM10（37.7 μg/m3）每增加一个四分位区间（IQR）浓度，儿童过敏性鼻炎调整后的OR值在特应性皮炎儿童中高于无特应性皮炎儿童中对应的OR值［PM1：OR=1.45，95%CI（1.26，1.66）vs. OR=1.33，95%CI（1.20，1.47）；PM2.5：OR=1.38，95%CI（1.23，1.56）vs. OR=1.32，95%CI（1.21，1.45）；PM10：OR=1.56，95%CI（1.31，1.86）vs. OR=1.46，95%CI（1.28，1.67）］。特应性皮炎与不同粒径PM暴露对儿童过敏性鼻炎的交互作用差异有显著的统计学意义（Z值=19.4，交互作用P值均<0.001）。在孕期和出生后第1年也观察到了类似的结果，且剂量反应关系的结果与logistic回归的结果具有一致性。综上，作为过敏性疾病进程重要环节的特应性皮炎可能会修饰大气颗粒物暴露与儿童过敏性鼻炎发生风险的关联。提示患特应性皮炎的儿童更应重视减少室外空气污染物的暴露，防止过敏性疾病的发生和进一步发展。.

BACKGROUND: Observational studies have reported associations between air pollutants and brain imaging-derived phenotypes (IDPs); however, whether this relationship is causal remains uncertain.
METHODS: We conducted bidirectional two-sample Mendelian randomization (MR) analyses to explore the causal relationships between 5 types of air pollutants (N=423,796 to 456,380 individuals) and 587 reliable IDPs (N=33,224 individuals). Two-step MR was also conducted to assess whether the identified effects are mediated through the modulation of circulating cytokines (N=8293).
RESULTS: We found genetic evidence supporting the association of nitrogen oxides (NOx) with mean intra-cellular volume fraction (ICVF) in the left uncinate fasciculus (IVW β=-0.42, 95 % CI -0.62 to -0.23, P=1.51×10-5) and mean fractional anisotropy (FA) in the left uncinate fasciculus (IVW β=-0.42, 95 % CI -0.62 to -0.21, P=4.89×10-5). In further two-step MR analyses, we did not find evidence that genetic predictions of any circulating cytokines mediated the association between NOx and IDPs.
CONCLUSIONS: This study provides evidence for the association between air pollutants and brain IDPs, emphasizing the importance of controlling air pollution to improve brain health.

UNASSIGNED: We evaluated the long-term effects of air pollution controls on health and health inequity among Chinese >45 years of age.
UNASSIGNED: Data were derived from the China Health Aging and Retirement Longitudinal Survey and the China National Environmental Monitoring Centre. Decreases in PM2.5 and PM10 were scaled to measure air quality controls. We used a quasi-experimental design to estimate the impact of air quality controls on self-reported health and health inequity. Health disparities were estimated using the concentration index and the horizontal index.
UNASSIGNED: Air pollution controls significantly improved self-reported health by 20% (OR 1.20, 95% CI, 1.02-1.42). The poorest group had a 40% (OR 1.41, 95% CI, 0.96-2.08) higher probability of having excellent self-reported health after air pollution controls. A pro-rich health inequity was observed, and the horizontal index decreased after air pollution controls.
UNASSIGNED: Air pollution controls have a long-term positive effect on health and health equity. The poorest population are the main beneficiaries of air pollution controls, which suggests policymakers should make efforts to reduce health inequity in air pollution controls.

UNASSIGNED: In recent years, the prevalence of obesity has continued to increase as a global health concern. Numerous epidemiological studies have confirmed the long-term effects of exposure to ambient air pollutant particulate matter 2.5 (PM2.5) on obesity, but their relationship remains ambiguous.
UNASSIGNED: Utilizing large-scale publicly available genome-wide association studies (GWAS), we conducted univariate and multivariate Mendelian randomization (MR) analyses to assess the causal effect of PM2.5 exposure on obesity and its related indicators. The primary outcome given for both univariate MR (UVMR) and multivariate MR (MVMR) is the estimation utilizing the inverse variance weighted (IVW) method. The weighted median, MR-Egger, and maximum likelihood techniques were employed for UVMR, while the MVMR-Lasso method was applied for MVMR in the supplementary analyses. In addition, we conducted a series of thorough sensitivity studies to determine the accuracy of our MR findings.
UNASSIGNED: The UVMR analysis demonstrated a significant association between PM2.5 exposure and an increased risk of obesity, as indicated by the IVW model (odds ratio [OR]: 6.427; 95% confidence interval [CI]: 1.881-21.968; P FDR = 0.005). Additionally, PM2.5 concentrations were positively associated with fat distribution metrics, including visceral adipose tissue (VAT) (OR: 1.861; 95% CI: 1.244-2.776; P FDR = 0.004), particularly pancreatic fat (OR: 3.499; 95% CI: 2.092-5.855; PFDR =1.28E-05), and abdominal subcutaneous adipose tissue (ASAT) volume (OR: 1.773; 95% CI: 1.106-2.841; P FDR = 0.019). Furthermore, PM2.5 exposure correlated positively with markers of glucose and lipid metabolism, specifically triglycerides (TG) (OR: 19.959; 95% CI: 1.269-3.022; P FDR = 0.004) and glycated hemoglobin (HbA1c) (OR: 2.462; 95% CI: 1.34-4.649; P FDR = 0.007). Finally, a significant negative association was observed between PM2.5 concentrations and levels of the novel obesity-related biomarker fibroblast growth factor 21 (FGF-21) (OR: 0.148; 95% CI: 0.025-0.89; P FDR = 0.037). After adjusting for confounding factors, including external smoke exposure, physical activity, educational attainment (EA), participation in sports clubs or gym leisure activities, and Townsend deprivation index at recruitment (TDI), the MVMR analysis revealed that PM2.5 levels maintained significant associations with pancreatic fat, HbA1c, and FGF-21.
UNASSIGNED: Our MR study demonstrates conclusively that higher PM2.5 concentrations are associated with an increased risk of obesity-related indicators such as pancreatic fat content, HbA1c, and FGF-21. The potential mechanisms require additional investigation.

Climate change is increasing the frequency and intensity of heatwaves, raising concerns about their detrimental effects on air quality. However, a role for heatwave-human-environment interactions in air pollution exacerbation has not been established. In the summer of 2022, record-breaking heatwaves struck China and Europe. In this study, we use integrated observational data and machine learning to elucidate the formation mechanism underlying one of the most severe ozone pollution seasons on record in central eastern China, an area that encompasses approximately half of China\'s total population and sown land. Our findings reveal that the worsened ozone and nitrogen dioxide pollution resulted from a mismatch between energy demand and supply, which was driven by both heatwaves and energy policy-related factors. The observed adverse heatwave-energy-environment feedback loop highlights the need for the diversification of clean energy sources, more resilient energy structures and power policies, and further emission control to confront the escalating climate challenge in the future.

Although epidemiological studies have demonstrated significant associations of long-term exposure to particulate matter (PM) air pollution with stroke, evidence on the long-term effects of PM exposure on cause-specific stroke incidence is scarce and inconsistent. We incorporated 33,282 and 33,868 individuals aged 35 to 75 years without a history of ischemic or hemorrhagic stroke at the baseline in 2014, who were followed up till 2021. Residential exposures to particulate matter with an aerodynamic diameter less than 2.5 μm (PM2.5) and particulate matter with an aerodynamic diameter less than 10 μm (PM10) for each participant were predicted using a satellite-based model with a spatial resolution of 1×1 km. We employed time-varying Cox proportional hazards models to assess the long-term effect of PM pollution on incident stroke. We identified 926 cases of ischemic stroke and 211 of hemorrhagic stroke. Long-term PM exposure was significantly associated with increased incidence of both ischemic and hemorrhagic stroke, with almost 2 times higher risk on hemorrhagic stroke. Specifically, a 10 μg/m³ increase in 3-year average concentrations of PM2.5 was linked to a hazard ratio (HR) of 1.35 (95% confidence interval (CI): 1.18-1.54) for incident ischemic stroke and 1.79 (95% CI: 1.36-2.34) for incident hemorrhagic stroke. The HR related to PM10, though smaller, remained statistically significant, with a HR of 1.25 for ischemic stroke and a HR of 1.51 for hemorrhagic stroke. The excess risks are larger among rural residents and individuals with lower educational attainment. The present cohort study contributed to the mounting evidence on the increased risk of incident stroke associated with long-term PM exposures. Our results further provide valuable evidence on the heightened sensitivity of hemorrhagic stroke to air pollution exposures compared with ischemic stroke.

Increased systemic oxidative stress, implicated in adverse pregnancy outcomes for both mothers and fetuses, has been associated with gestational exposure to air pollutants such as polycyclic aromatic hydrocarbons (PAHs), fine particulate matter (PM2.5), and nitrogen dioxide (NO2). However, it is unclear whether exposure to pollutants at levels below the current air quality standards can increase oxidative stress in pregnant women. In a cohort of 305 pregnant persons residing in western New York, we examined the association between exposure to PM2.5, NO2, and PAHs (measured as urinary 1-hydroxypyrene) and urinary biomarkers of oxidative stress (malondialdehyde [MDA] and 8-hydroxy-2\'-deoxyguanosine [8-OHdG]) measured in each trimester. After controlling for gestational stage, maternal age, lifestyles, and socioeconomic factors, each interquartile range (IQR) increase in 1-hydroxypyrene concentration (65.8 pg/ml) was associated with a 7.73% (95%CI: 3.18%,12.3%) higher in MDA levels throughout the pregnancy and in the first and second trimester. An IQR increase in PM2.5 concentration (3.20 μg/m3) was associated with increased MDA levels in the first trimester (8.19%, 95%CI: 0.28%,16.1%), but not the 2nd (-7.99%, 95% CI: -13.8%, -2.23%) or 3rd trimester (-2.81%, 95% CI: -10.0%, 4.38%). The average cumulative PM2.5 exposures in the 3-7 days before urine collection were associated with increased 8-OHdG levels during the second trimester, with the largest difference (22.6%; 95% CI: 3.46%, 41.7%) observed in relation to a one IQR increase in PM2.5 concentration in the previous 7 days. In contrast, neither oxidative stress biomarker was associated with NO2 exposure. Observed in pregnant women exposed to low-level air pollution, these findings expanded previously reported associations between systemic oxidative stress and high-level PM2.5 and PAH concentrations. Further, the first and second trimesters may be a susceptible window during pregnancy for oxidative stress responses to air pollution exposure.

UNASSIGNED: Ozone pollution is associated with cardiovascular disease mortality, and there is a high correlation between different pollutants. This study aimed to assess the association between ozone and cardiovascular disease deaths and the resulting disease burden in Nanjing, China.
UNASSIGNED: A total of 151,609 deaths from cardiovascular disease were included in Nanjing, China from 2013 to 2021. Daily data on meteorological and air pollution were collected to apply a generalized additional model with multiple pollutants to perform exposure-response analyses, stratification analysis, and evaluation of excess deaths using various standards.
UNASSIGNED: In the multi-pollutant model, an increase of 10 μg/m3 in O3 was significantly associated with a 0.81% (95%CI: 0.49, 1.12%) increase in cardiovascular disease deaths in lag05. The correlation weakened in both the single-pollutant model and two-pollutant models, but remained more pronounced in females, the older group, and during warm seasons. From 2013 to 2021, the number of excess deaths attributed to ozone exposure in cardiovascular disease continued to rise with an increase in ozone concentration in Nanjing. If the ozone concentration were to be reduced to the WHO standard and the minimum level, the number of deaths would decrease by 1,736 and 10,882, respectively.
UNASSIGNED: The risk of death and excess deaths from cardiovascular disease due to ozone exposure increases with higher ozone concentration. Reducing ozone concentration to meet WHO standards or lower can provide greater cardiovascular disease health benefits.

BACKGROUND: Environmental factors greatly impact infectious disease-related mortality, yet there\'s a lack of comprehensive global studies on the contemporary burden and trends. This study aims to evaluate the global burden and trends of infectious disease mortality caused by air pollution, unsafe water, poor sanitation, and non-optimal temperature across Socio-Demographic Index (SDI) regions from 1990 to 2019.
METHODS: This observational study utilized data from the Global Burden of Diseases Study to examine mortality rates from infectious diseases attributed to environmental risk factors between 1990 and 2019, including air pollution, unsafe water, sanitation, handwashing facilities (UWSH), and non-optimal temperatures. Age-standardized mortality rates (ASMRs) and estimated annual percentage change (EAPC) were utilized to present infectious disease mortality, and its trajectory influenced by environmental risk factors over the years. Nonlinear regression was conducted to explore the association between the SDI and ASMRs across regions from 1990 to 2019.
RESULTS: In 2019, global infectious disease deaths linked to air pollution, UWSH, and non-optimal temperature reached a startling 2,556,992. Disease mortality varied widely across SDI regions, with the highest number of deaths due to air pollution and UWSH in Low SDI regions, and deaths from non-optimal temperature primarily in High SDI regions. Age disparities emerged, with children under five and the elderly most affected. However, an increasing mortality trend was observed among seniors (65-69, 75-79, and over 80) in High SDI regions due to enteric infections linked to UWSH. Globally, a consistent decrease in ASMR was seen from 1990 to 2019 for all diseases connected to these factors, except for respiratory infections linked to non-optimal temperature.
CONCLUSIONS: Our study underscores the significant impact of air pollution, UWSH, and non-optimal temperatures on global infectious disease mortality, particularly among vulnerable groups such as children and the elderly. It\'s important to tackle these challenges with targeted interventions aiming to enhance environmental quality, improve water and sanitation systems, and control extreme temperatures. In addition, international cooperation is essential for bridging regional disparities and driving global public health initiatives forward, thereby helping achieve Sustainable Development Goals more effectively.