Dry Eye and Visual Display Terminal-Related Symptoms among University Students during the Coronavirus Disease Pandemic.

PURPOSE: To evaluate dry eye (DE) and subjective visual display terminal (VDT)-related symptoms in university students who moved their classes online due to the COVID-19 pandemic. METHODS: Cross-sectional study of students who were taking online classes. In May 2020, the participants completed a Dry Eye Questionnaire (DEQ-5) and a self-report survey, which included demographics, medical history, information on the use of VDT and presence of VDT-related symptoms. Participants were classified as having mild/moderate (7-12) or severe (>12) DE symptoms based on their DEQ-5 score. The associations between severe DE symptoms and relevant factors were also evaluated. RESULTS: The data of 1450 eligible students were analyzed. The mean age of the participants was 21.1 (2.7) years. 42.8% of the participants had mild/moderate DE symptoms, whereas 34.7% had severe symptoms. Associated factors for severe DE were female sex (OR = 2.57, CI [1.97-3.35]), allergic disease (OR = 1.63, CI [1.24-2.13]), previous dry eye diagnosis (OR = 13.49, CI [7.10-25.63]), keratoconus (OR = 5.56, CI [1.27-24.44], contact lens use (OR = 1.77, CI [1.24-2.53]) and duration of VDT use (OR = 1.02, CI [1.01-1.05]). Prior to the pandemic, the mean reported duration of VDT use was 9.8 (4.7) hours; this increased to 15.9 (5.8) hours during the online classes (p < .001). 80.6% of the participants reported a global increase in VDT-related symptoms. CONCLUSION: Students taking online classes had a high frequency of DE symptoms. They also reported a significant increase in VDT-related symptoms. DE should be considered as an emerging health problem among the young population, which is probably related to the recent changes in lifestyle.

High frequency of digital eye strain and dry eye disease in teleworkers during the coronavirus disease (2019) pandemic.

Objectives. This study aimed to evaluate visual display terminal (VDT)-related digital eye strain (ES) and dry eye disease (DED) symptoms in subjects whose work was changed to teleworking (TW) during the coronavirus pandemic. Methods. A digital self-reported survey was conducted on subjects in TW, including demographics, medical history, VDT time and ES-related symptoms before and during the pandemic and DED (dry eye questionnaire 5 [DEQ-5] questionnaire). Results. A total of 1797 questionnaires were analyzed. Mean age was 40.5 (SD 11.1) years, and 69.9% were female. The mean number of TW weeks was 10.2 (SD 3.0). The total VDT total hours increased from 7.4 (SD 3.3) to 9.5 (SD 3.3) (p < 0.001). All ES symptoms presented a significant increase (p < 0.001). The mean DEQ-5 score was 8.3 (SD 4.9). The oldest group presented lower values, and women had a higher score (p < 0.001). Additionally, 28.6% of the subjects were classified with severe DED, and the variables associated with a logistic regression model were total VDT hours, female gender, refractive surgery, rosacea, depression, previous DED, keratoconus and blepharitis. Conclusions. The number of VDT hours seemed to be a relevant factor for increase in ES symptoms and a high prevalence of DED during the pandemic period.

Chronic Low-Level Lead Exposure Increases Mesenteric Vascular Reactivity: Role of Cyclooxygenase-2-Derived Prostanoids.

Lead (Pb) exposure causes hazardous effects as hypertension and other cardiovascular diseases. We evaluated whether chronic Pb exposure alters the peripheral vascular resistance measuring the vascular reactivity of mesenteric resistance arteries in rats to identify the underlying mechanisms that are associated to the development of Pb-induced hypertension. Mesenteric resistance arteries from lead-treated and untreated Wistar rats (1st dose: 10 µg/100 g; subsequent doses: 0.125 µg/100 g, intramuscular, 30 days) were used. Contractile responses to phenylephrine increased, while acetylcholine and sodium nitroprusside-induced relaxation was not affected by lead treatment. Endothelium removal and inhibition of NO synthase by L-NAME similarly enhanced the response to phenylephrine in untreated and lead-treated rats. The antioxidants apocynin and superoxide dismutase (SOD) did not affect vasoconstriction in either group. The vascular expression of cyclooxygenase-2 (COX-2) protein increased after lead exposure. The respective non-specific or specific COX-2 inhibitors indomethacin and NS398 reduced more strongly the response to phenylephrine in treated rats. Antagonists of EP1 (SC19220), TP (SQ29548), IP (CAY10441) and angiotensin II type 1 (losartan) receptors reduced vasoconstriction only in treated rats. These conclusions present further evidence that lead, even in small concentration, produces cardiovascular hazards being an environmental contaminant that account for lead-induced hypertension.

Aluminum exposure at human dietary levels promotes vascular dysfunction and increases blood pressure in rats: A concerted action of NAD(P)H oxidase and COX-2.

Aluminum (Al) is a non-essential metal and a significant environmental contaminant and is associated with a number of human diseases including cardiovascular disease. We investigated the effects of Al exposure at doses similar to human dietary levels on the cardiovascular system over a 60day period. Wistar male rats were divided into two major groups and received orally: 1) Low aluminum level - rats were subdivided and treated for 60days as follows: a) Untreated - ultrapure water; b) AlCl3 at a dose of 8.3mg/kg bw for 60days, representing human Al exposure by diet; and 2) High aluminum level - rats were subdivided and treated for 42days as follows: C) Untreated - ultrapure water; d) AlCl3 at 100mg/kg bw for 42days, representing a high level of human exposure to Al. Effects on systolic blood pressure (SBP) and vascular function of aortic and mesenteric resistance arteries (MRA) were studied. Endothelium and smooth muscle integrity were evaluated by concentration-response curves to acetylcholine (ACh) and sodium nitroprusside. Vasoconstrictor responses to phenylephrine (Phe) in the presence and absence of endothelium and in the presence of the NOS inhibitor L-NAME, the potassium channels blocker TEA, the NAD(P)H oxidase inhibitor apocynin, superoxide dismutase (SOD), the non-selective COX inhibitor indomethacin and the selective COX-2 inhibitor NS 398 were analyzed. Vascular reactive oxygen species (ROS), lipid peroxidation and total antioxidant capacity, were measured. The mRNA expressions of eNOS, NAD(P)H oxidase 1 and 2, SOD1, COX-2 and thromboxane A2 receptor (TXA-2 R) were also investigated. Al exposure at human dietary levels impaired the cardiovascular system and these effects were almost the same as Al exposure at much higher levels. Al increased SBP, decreased ACh-induced relaxation, increased response to Phe, decreased endothelial modulation of vasoconstrictor responses, the bioavailability of nitric oxide (NO), the involvement of potassium channels on vascular responses, as well as increased ROS production from NAD(P)H oxidase and contractile prostanoids mainly from COX-2 in both aorta and mesenteric arteries. Al exposure increased vascular ROS production and lipid peroxidation as well as altered the antioxidant status in aorta and MRA. Al decreased vascular eNOS and SOD1 mRNA levels and increased the NAD(P)H oxidase 1, COX-2 and TXA-2 R mRNA levels. Our results point to an excess of ROS mainly from NAD(P)H oxidase after Al exposure and the increased vascular prostanoids from COX-2 acting in concert to decrease NO bioavailability, thus inducing vascular dysfunction and increasing blood pressure. Therefore, 60-day chronic exposure to Al, which reflects common human dietary Al intake, appears to pose a risk for the cardiovascular system.

The cessation of the long-term exposure to low doses of mercury ameliorates the increase in systolic blood pressure and vascular damage in rats.

This study aimed to verify whether a prolonged exposure to low-level mercury promotes haemodynamic disorders and studied the reversibility of this vascular damage. Rats were divided into seven groups: three control groups received saline solution (im) for 30, 60 or 90 days; two groups received HgCl2 (im, first dose, 4.6µg/kg, subsequent doses 0.07µg/kg/day) for 30 or 60 days; two groups received HgCl2 for 30 or 60 days (im, same doses) followed by a 30-day washout period. Systolic blood pressure (SBP) was measured, along with analysis of vascular response to acetylcholine (ACh) and phenylephrine (Phe) in the absence and presence of endothelium, a nitric oxide (NO) synthase inhibitor, an NADPH oxidase inhibitor, superoxide dismutase, a non-selective cyclooxygenase (COX) inhibitor and an AT1 receptor blocker. Reactive oxygen species (ROS) levels and antioxidant power were measured in plasma. HgCl2 exposure for 30 and 60 days: a) reduced the endothelium-dependent relaxation; b) increased the Phe-induced contraction and the contribution of ROS, COX-derived vasoconstrictor prostanoids and angiotensin II acting on AT1 receptors to this response while the NO participation was reduced; c) increased the oxidative stress in plasma; d) increased the SBP only after 60 days of exposure. After the cessation of HgCl2 exposure, SBP, endothelium-dependent relaxation, Phe-induced contraction and the oxidative stress were normalised, despite the persistence of the increased COX-derived prostanoids. These results demonstrated that long-term HgCl2 exposure increases SBP as a consequence of vascular dysfunction; however, after HgCl2 removal from the environment the vascular function ameliorates.

Aluminum exposure for one hour decreases vascular reactivity in conductance and resistance arteries in rats.

AIMS: Aluminum (Al) is an important environmental contaminant; however, there are not enough evidences of Al-induced cardiovascular dysfunction. We investigated the effects of acute exposure to aluminum chloride (AlCl3) on blood pressure, vascular reactivity and oxidative stress. METHODS AND RESULTS: Male Wistar rats were divided into two groups: Untreated: vehicle (ultrapure water, ip) and AlCl3: single dose of AlCl3 (100mg/kg,ip). Concentration-response curves to phenylephrine in the absence and presence of endothelium, the nitric oxide synthase inhibitor l-NAME, the potassium channel blocker tetraethylammonium, and the NADPH oxidase inhibitor apocynin were performed in segments from aortic and mesenteric resistance arteries. NO released was assessed in aorta and reactive oxygen species (ROS), malondialdehyde, non-protein thiol levels, antioxidant capacity and enzymatic antioxidant activities were investigated in plasma, aorta and/or mesenteric arteries. After one hour of AlCl3 exposure serum Al levels attained 147.7±25.0µg/L. Al treatment: 1) did not affect blood pressure, heart rate and vasodilator responses induced by acetylcholine or sodium nitroprusside; 2) decreased phenylephrine-induced vasoconstrictor responses; 3) increased endothelial modulation of contractile responses, NO release and vascular ROS production from NADPH oxidase; 4) increased plasmatic, aortic and mesenteric malondialdehyde and ROS production, and 5) decreased antioxidant capacity and affected the antioxidant biomarkers non-protein thiol levels, glutathione peroxidase, glutathione-S-transferase, superoxide dismutase and catalase enzymatic activities. CONCLUSION: AlCl3-acute exposure reduces vascular reactivity. This effect is associated with increased NO production, probably acting on K+ channels, which seems to occur as a compensatory mechanism against Al-induced oxidative stress. Our results suggest that Al exerts toxic effects to the vascular system.

Toxic effects of mercury on the cardiovascular and central nervous systems.

Environmental contamination has exposed humans to various metal agents, including mercury. This exposure is more common than expected, and the health consequences of such exposure remain unclear. For many years, mercury was used in a wide variety of human activities, and now, exposure to this metal from both natural and artificial sources is significantly increasing. Many studies show that high exposure to mercury induces changes in the central nervous system, potentially resulting in irritability, fatigue, behavioral changes, tremors, headaches, hearing and cognitive loss, dysarthria, incoordination, hallucinations, and death. In the cardiovascular system, mercury induces hypertension in humans and animals that has wide-ranging consequences, including alterations in endothelial function. The results described in this paper indicate that mercury exposure, even at low doses, affects endothelial and cardiovascular function. As a result, the reference values defining the limits for the absence of danger should be reduced.

Activation of K+ channels and Na+/K+ ATPase prevents aortic endothelial dysfunction in 7-day lead-treated rats.

Seven day exposure to a low concentration of lead acetate increases nitric oxide bioavailability suggesting a putative role of K+ channels affecting vascular reactivity. This could be an adaptive mechanism at the initial stages of toxicity from lead exposure due to oxidative stress. We evaluated whether lead alters the participation of K+ channels and Na+/K+)-ATPase (NKA) on vascular function. Wistar rats were treated with lead (1st dose 4 µg/100 g, subsequent doses 0.05 µg/100g, im, 7 days) or vehicle. Lead treatment reduced the contractile response of aortic rings to phenylephrine (PHE) without changing the vasodilator response to acetylcholine (ACh) or sodium nitroprusside (SNP). Furthermore, this treatment increased basal O2⁻ production, and apocynin (0.3 µM), superoxide dismutase (150 U/mL) and catalase (1000 U/mL) reduced the response to PHE only in the treated group. Lead also increased aortic functional NKA activity evaluated by K+-induced relaxation curves. Ouabain (100 µM) plus L-NAME (100 µM), aminoguanidine (50 µM) or tetraethylammonium (TEA, 2 mM) reduced the K+-induced relaxation only in lead-treated rats. When aortic rings were precontracted with KCl (60 mM/L) or preincubated with TEA (2 mM), 4-aminopyridine (4-AP, 5 mM), iberiotoxin (IbTX, 30 nM), apamin (0.5 µM) or charybdotoxin (0.1 µM), the ACh-induced relaxation was more reduced in the lead-treated rats. Additionally, 4-AP and IbTX reduced the relaxation elicited by SNP more in the lead-treated rats. Results suggest that lead treatment promoted NKA and K+ channels activation and these effects might contribute to the preservation of aortic endothelial function against oxidative stress.