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Epidemiological studies show a positive association between air pollution and age-related cataracts, but the pathogenic mechanism remains unclear. This study first demonstrates that fine particulate matter (PM 2.5) induces ferroptosis in the lens, leading to morphological and functional disorders, through human, animal, and cellular samples. In 3-week PM 2.5 -exposed rat models (10 µl 1 mg/ml PM 2.5 suspension per eye, 4 times a day), we find that many vacuoles form in the lens equatorial region by analysis of haematoxylin and eosin staining after PM 2.5 exposure. Using iron and glutathione (GSH) assay kits, we found increased Fe2+ contents and decreased GSH levels in PM 2.5 -exposed rats' lenses. Additionally, the lipid peroxide 4-hydroxynonenal (4-HNE) was also found to be elevated with immunoblot, suggesting ferroptosis is involved. Ferroptosis was also observed in human lens epithelial cells treated with 25, 50, and 100 µg/ml PM 2.5 suspension for 24 h, accompanied by decreased cell viability and migration. Furthermore, we collect about 60 human lens anterior capsule (HLAC) samples for RNA-seq. The results show that compared to HLACs from areas with PM 2.5 concentration ≤30 μg/m³, ferroptosis-related genes expression of those from areas with PM 2.5 concentration ≥35 μg/m³ are significantly altered, such as glutathione peroxidase 4 and STEAP family member 3. Also, human lens in areas with high PM 2.5 concentrations showed elevated levels of transferrin receptor and 4-HNE with immunoblot, and down-regulated expression of connexin 43 (Cx43) through immunofluorescent. These results demonstrate that ferroptosis plays a key role in PM 2.5 -induced cataractogenesis. [Display omitted] • Cataracts, the leading cause of blindness, can be promoted by PM 2.5 exposure. • PM 2.5 exposure can cause structural and metabolic disorders of the lens in rats. • Ferroptosis plays an important role in rats' lens damage induced by PM 2.5 exposure. • The structure of human lens epithelial cells in polluted area are disordered. • RNA-seq indicates the involvement of ferroptosis in PM2.5-related cataractogenesis. [ABSTRACT FROM AUTHOR]

To monitor the body burden of persistent organic pollutants in mothers and infants living in proximity to a 10-year-old municipal waste incinerator (MWI), levels of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polychlorinated biphenyls (PCBs) in the breast milk of mothers were evaluated, and the estimated daily intake (EDI) level of these pollutants in infants was assessed. In total, 14 mothers from the exposure area and 18 mothers from a control area were recruited for this study. In addition, the levels of 17 PCDD/F congeners and 18 PCB congeners in the breast milk of the mothers were estimated, and risk assessment for their infants by calculating their EDI levels was performed. The mean levels of ΣPCDD/Fs and TEQ-ΣPCDD/Fs in the breast milk of the exposure group were significantly greater than those of the control group (3.36 vs. 1.47 pg/g wet weight; and 0.24 vs. 0.12 pg TEQ/g wet weight, respectively; p < 0.05). With respect to PCBs, the mean levels of the total PCBs (ΣPCBs) and non-dioxin like-PCBs (ΣNDL-PCBs) in the exposure group were significantly greater than those in the control group (269 vs. 141 pg/g wet weight; 230 vs. 115 pg/g wet weight, respectively; p < 0.05). The mean levels of ΣPCDD/Fs and TEQ-ΣPCDD/Fs were positively correlated with the inhabit time of the exposure group (r = 0.636, r = 0.629, p < 0.05, respectively). The mean EDI level of the exposure group in infants was significantly greater than that of the control group (22.0 vs. 13.0 pg TEQ/kg bw day; p < 0.05). In conclusion, mothers and their breast-fed infants living in proximity to the 10-year-old MWI located in the Zhejiang Province of China exhibited a significantly higher body burden of PCDD/Fs and PCBs compared to those living in the control area. Image 1 • Mothers residing near a MWI exhibited a higher body burden of PCDD/Fs and PCBs. • Levels of PCDD/Fs in the breast milk of mothers were positively correlated with the inhabit time. • The infants' EDI of the pollutants was higher in the exposure area compared to the control area. Mothers and their breast-fed infants residing near a municipal waste incinerator exhibited a higher body burden of PCDD/Fs and PCBs compared to those residing in the control area. [ABSTRACT FROM AUTHOR]

Abstract The purpose of this study is to investigate the potential associations between air pollution and dry eye disease (DED). Data of outdoor air pollutants and meteorology as well as outpatient visits for DED were collected. A time-stratified case-crossover approach was used to analyze the associations between ambient air pollutants and outpatient visits for DED. Among the 5062 DED patients studied, 65.45% were female and 34.55% were male. In the single-pollutant model, significant associations were observed between an increase of 10 μg/m3 in the concentrations of fine-particulate matter with a median aerometric diameter of less than 10 μm (PM 10), fine-particulate matter with a median aerometric diameter of less than 2.5 μm (PM 2.5), sulfur dioxide (SO 2), nitrogen dioxide (NO 2), and carbon monoxide (CO) and outpatient visits for DED. These results were consistent with those of the multipollutant model. The strongest associations between air pollutants and patient visits were observed during the cold season and in patients aged 21–40. The significant association between air pollutants (PM 10 , PM 2.5 , SO 2 , NO 2 , and CO) and DED outpatient visits indicates the importance of increased environmental protection. Graphical abstract Image 1 Highlights • Significant associations between air pollution and dry eye disease were observed. • The most susceptible populations were those aged 21–40. • The impact of air pollution on dry eye disease was stronger in the cold season. Outpatient visits for DED were significantly associated with air pollutants in Hangzhou, China. [ABSTRACT FROM AUTHOR]

BACKGROUND Conjunctivitis, one of the most common ocular surface diseases, can be caused by many factors. OBJECTIVES The objective of this study was to investigate the potential association between conjunctivitis and air pollutants. MATERIALS AND METHODS Data of 9737 outpatient visits for conjunctivitis from July 1, 2014 to June 30, 2016 were obtained from the Eye Center of the Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China. The data were linked to data on the concentrations of carbon monoxide (CO), nitrogen dioxide (NO 2 ), ozone (O 3 ), sulfur dioxide (SO 2 ), and fine particulate matter with a median aerometric diameter of less than 10 and 2.5 μm (PM 10 and PM 2.5 , respectively), which were obtained from the Environmental Protection Department of Zhejiang Province. A time-stratified case-crossover study design and conditional logistic regression were applied to analyze the association between air pollutants and outpatient visits for conjunctivitis. RESULTS A 10 μg/m 3 increase in PM 10 , PM 2.5 , SO 2 , NO 2 , and CO concentrations on the same day as the hospital visit or on lag days before the hospital visit date was associated with outpatient visits for conjunctivitis. The strongest association was observed between SO 2 and conjunctivitis patients aged 2–5 years. Variation occurs between warm and cold seasons, between genders, and among different age groups. CONCLUSIONS Our study provided evidence that outpatient visits for conjunctivitis were significantly associated with air pollution in Hangzhou, China. [ABSTRACT FROM AUTHOR]

Corneal epithelium integrity depends on continuous self-renewing of epithelium and connections between adjacent cells or between the cells and the basement membrane. Self-renewing epithelium cells mainly arise from the continuous proliferation and differentiation of the basal layer and limbal stem cells. The aim of the present study was to generate a bioactive, thermosensitive chitosan–gelatin hydrogel (CHI hydrogel) by incorporating exogenous recombinant human stromal cell–derived factor-1 alpha (SDF-1 alpha) for corneal epithelium regeneration. The exogenous SDF-1 alpha could enhance the stem cells proliferation, chemotaxis and migration, and the expression levels of related genes were significantly elevated in LESCs and mesenchymal stem cells (MSCs) in vitro. Moreover, the MSCs promoted the proliferation and maintained the corneal fate of the LESCs. The rat alkali injury model was used for in vivo study. The injured eyes were covered with CHI hydrogel alone or rhSDF-1 alpha-loaded CHI hydrogel. All rats were followed for 13 days. Histological examination showed that the SDF-1 alpha/CHI hydrogel complex group had a nearly normal thickness; moreover, it was also found that this group could upregulate the expression of some genes and had more ΔNp63-positive cells. The SDF-1 alpha/CHI hydrogel complex group had a more tightly arranged epithelium compared with the control group using transmission electron microscopy (TEM). The mechanism for this may have involved the activation of stem cell homing and the secretion of growth factors via the SDF-1/CXCR4 chemokine axis. Therefore, SDF-1 alpha/CHI hydrogel complexes could provide a new idea for the clinical application. Statement of significance The clarity of cornea is important for normal vision. The loss or dysfunction of LESCs leads to the impairment of corneal epithelium. The complete regeneration of corneal epithelium has not been achieved. Our study demonstrated that the incorporation of rhSDF-1 alpha with CHI hydrogel accelerated corneal epithelium reconstruction with more native structural and functional properties. The mechanism may involve in inducing proliferation and migration of the LESCs and MSCs to the injury site via the SDF-1/CXCR4 chemokine axis. Therefore, SDF-1 alpha/CHI hydrogel complexes could be a practical application for clinical therapy. [ABSTRACT FROM AUTHOR]

Purpose To investigate particulate matter (PM2.5)-induced damage to human corneal epithelial cells (HCECs) and to determine the underlying mechanisms. Methods HCECs were exposed to PM2.5 at a series of concentrations for various periods. Cell viability was measured by using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell proliferation was evaluated via 5-ethynyl-2’-deoxyuridine (EdU) analysis, while autophagy was determined by immunofluorescence and Western blot. Results PM2.5-induced cell damage of HCECs occurred in a time- and dose-dependent manner. Decreased cell viability and proliferation as well as increased apoptosis were observed in HCECs after PM2.5 exposure for 24 h. Autophagy in HCECs was slightly inhibited in the early stage (before 4 h) of exposure but significantly activated in the late stage (after 24 h), as evidenced by a decrease in the former and increase in the latter of the expression of the autophagy-associated markers LC3B, ATG5, and BECN1. Interestingly, rapamycin, an autophagy activator, attenuated early-stage but aggravated late-stage PM2.5-induced cell damage, suggesting that the role of autophagy in HCECs may change over time during PM2.5 exposure. In addition, in the early stage, the expression of LC3B and ATG5 increased in cells co-treated with rapamycin and PM2.5 compared to rapamycin-only or PM2.5-only treated cells, suggesting that autophagy may benefit cell viability after PM2.5 exposure. Conclusions The results indicate the potential role of autophagy in the treatment of PM2.5-induced ocular corneal diseases and provide direct evidence for the cytotoxicity, possibly involving an autophagic process, of PM2.5 in HCECs. [ABSTRACT FROM AUTHOR]

Air pollution could be a risk factor for the development of pterygium. This study aimed to investigate the potential associations between outpatient visits for pterygium and air pollutants. Using a time-stratified case-crossover design, the data of 3017 outpatients with pterygium visiting an eye center in Hangzhou, China, and the air pollution data of the Environmental Protection Department of Zhejiang Province between July 1, 2014, and November 30, 2019, were examined. The relationships between the air pollutants nitrogen dioxide (NO 2), sulfur dioxide (SO 2), ozone, and fine particulate matter (PM) with median aerometric diameter <2.5 μm (PM 2.5) and <10 μm (PM 10) and outpatient visits for primary pterygium were assessed using single- and multiple-pollutant models. Significant associations between outpatient visits for pterygium and air pollutants (PM 2.5 , PM 10 , SO 2 , and NO 2) were observed. Younger patients were found to be more sensitive to air pollution. Interestingly, the younger female patients with pterygium were more vulnerable to PM 2.5 exposure during the warm season, while the younger male patients with pterygium were more sensitive to NO 2 during the cold season. Significant effects were also observed between the pterygium outpatients and PM 2.5 (odds ratio [OR] = 1.06, P = 0.02), PM 10 (OR = 1.04, P = 0.01), and SO 2 (OR = 1.26, P = 0.01) during the warm season, as well as NO 2 (OR = 1.06, P = 0.01) during the cold season. Our study provides evidence that outpatient visits for pterygium are positively associated with increases in the air pollutants PM 2.5 , PM 10 , SO 2 , and NO 2 , revealing the important role of air pollution in the occurrence and development of pterygium. [Display omitted] • Air pollutants are in significant associations with outpatient visits for pterygium. • Younger pterygium patients are more sensitive to air pollution. • The female pterygium patients are more vulnerable to PM 2.5 during the warm season. • The male pterygium patients are more sensitive to NO 2 during the cold season. [ABSTRACT FROM AUTHOR]