Changes in thrombosis-related parameters after AstraZeneca COVID-19 vaccination in a male volunteer: a case report.

BACKGROUND: We speculated that subclinical thrombosis may occur frequently through crosstalk between immune/inflammatory reactions and hemostasis after corona virus disease-2019 (COVID-19) vaccination. To test this hypothesis, we measured thrombosis-related parameters after COVID-19 vaccination in a volunteer for 21 days. CASE PRESENTATION: The following parameters were measured in a 72-year-old Korean man at 1 day before vaccination and on days 1, 3, 7, 14, and 21 post vaccination (AstraZeneca COVID-19 vaccine: ChAdOx1-S/nCoV-19, CTMAV563): complete blood count, platelet indices, thrombin receptor-activating peptide-induced platelet aggregation, prothrombin time, activated partial thromboplastin time, D-dimer, thrombin-antithrombin III complex (TAT), plasmin-α2 antiplasmin complex (PAP), von Willebrand factor (vWF) antigen and activity, plasminogen activator inhibitor-1 (PAI-1), protein C and protein S antigen and activity, lupus anticoagulant, fibrinogen degradation product, and plasminogen. We found that the TAT had significantly increased from 0.7 ng/mL (baseline) to 21.7 ng/mL (day 1). There was a transient increase in the PAI-1 level from 7.2 ng/mL (baseline) to 10.9 ng/mL (day 3), followed by a decrease in PAP level from 0.9 ng/mL (baseline) to 0.3 µg/mL (day 7), suggesting that plasmin generation is suppressed by PAI-1. CONCLUSIONS: Increased thrombotic factors (such as decreased protein S) and decreased fibrinolytic activity due to increased PAI-1 were potential factors causing thrombogenesis after COVID-19 vaccination. Sequential measurement of platelet indices, TAT, PAP, protein C, protein S, vWF, D-dimer, and PAI-1 following COVID-19 vaccination was informative.

The effects of nonyl phenoxypolyethoxyl ethanol on cell damage pathway gene expression in SK-NSH cells.

BACKGROUND/AIMS: Most pesticide formulations contain both chief and additive ingredients. But, the additives may not have been tested as thoroughly as the chief ingredients. The surfactant, nonyl phenoxypolyethoxylethanol (NP40), is an additive frequently present in pesticide formulations. We investigated the effects of NP40 and other constituents of a validamycin pesticide formulation on cell viability and on the expression of genes involved in cell damage pathways. METHODS: The effects of validamycin pesticide ingredients on cell viability and of NP40 on the mRNA expression of 80 genes involved in nine key cellular pathways were examined in the human neuroblastoma SK-N-SH cell line. RESULTS: The chemicals present in the validamycin pesticide formulation were cytotoxic to SK-N-SH cells and NP40 showed the greatest cytotoxicity. A range of gene expression changes were identified, with both up- and down-regulation of genes within the same pathway. However, all genes tested in the necrosis signaling pathway were down-regulated and all genes tested in the cell cycle checkpoint/arrest pathway were up-regulated. The median fold-change in gene expression was significantly higher in the cell cycle checkpoint/arrest pathway than in the hypoxia pathway category (p = 0.0064). The 70 kDa heat shock protein 4 gene, within the heat shock protein/unfolded protein response category, showed the highest individual increase in expression (26.1-fold). CONCLUSIONS: NP40 appeared to be particularly harmful, inducing gene expression changes that indicated genotoxicity, activation of the cell death (necrosis signaling) pathway, and induction of the 70 kDa heat shock protein 4 gene.

Common Pesticides Used in Suicide Attempts Following the 2012 Paraquat Ban in Korea.

To determine the change in pesticides used during suicide attempts after the 2012 paraquat (PQ) ban, we evaluated the annual number of suicide attempts by pesticide ingestion between 2011 and 2014. We extracted demographic, clinical outcome, and pesticide class data from the medical records of 1,331 patients that attempted suicide by pesticide ingestion. Pesticides were sorted into 5 groups: herbicides, insecticides, fungicides, other pesticides, and combined pesticides. Each group was subdivided into various classes based on publications by the respective Resistance Action Committees. The chi-square test for trends was used to compare the annual incidence of categorical variables. The total number of suicide attempts decreased each year, from 399 in 2011 to 245 in 2014. Simultaneously, PQ ingestion decreased from 253 patients in 2011 to 60 in 2014. The proportion of PQ to pesticides also decreased from 63.4% in 2011 to 24.5% in 2014. Furthermore, the rate of decrease in the proportion of PQ to all herbicide categories increased by calendar year. In conclusion, there is a significant trend in increased annual number of suicides and proportion of suicides using glyphosates and glufosinates versus total herbicides. However, the number of suicide attempts using glyphosate and glufosinate is lower than that using PQ. The ratio of persons completing suicide to those attempting suicide after pesticide ingestion has decreased every year after the PQ ban.

Idiopathic erythrocytosis in a patient on chronic hemodialysis.

A 78-year-old man on hemodialysis presented to our hospital with erythrocytosis. He had started hemodialysis 4 years previously, with a hemoglobin level of 9.8 g/dL, and was administered erythropoiesis stimulating agents and ferrous sulfate. Two years previously, his hemoglobin level increased to 14.5 g/dL and the treatment for anemia was discontinued. He continued hemodialysis thrice weekly; however, the hemoglobin level had increased to 17.0 g/dL at the time of presenting to our hospital. His serum erythropoietin level was 31.4 mIU/mL (range, 3.7-31.5 mIU/mL), carboxyhemoglobin level was 0.6% (range, 0-1.5%), and oxygen saturation in ambient air was 95.4%. The JAK2 V617F mutation was not observed and other bone marrow abnormalities were not identified. The patient was diagnosed with bladder cancer and a transurethral resection was performed. Eight months after the treatment of bladder cancer, his hemoglobin level was 15.1 g/dL, and he was diagnosed with idiopathic erythrocytosis.

Effects of formaldehyde on mitochondrial dysfunction and apoptosis in SK-N-SH neuroblastoma cells.

Methanol ingestion is neurotoxic in humans due to its metabolites, formaldehyde and formic acid. Here, we compared the cytotoxicity of methanol and its metabolites on different types of cells. While methanol and formic acid did not affect the viability of the cells, formaldehyde (200-800 µg/mL) was strongly cytotoxic in all cell types tested. We investigated the effects of formaldehyde on oxidative stress, mitochondrial respiratory functions, and apoptosis on the sensitive neuronal SK-N-SH cells. Oxidative stress was induced after 2 h of formaldehyde exposure. Formaldehyde at a concentration of 400 µg/mL for 12 h of treatment greatly reduced cellular adenosine triphosphate (ATP) levels. Confocal microscopy indicated that the mitochondrial membrane potential (MMP) was dose-dependently reduced by formaldehyde. A marked and dose-dependent inhibition of mitochondrial respiratory enzymes, viz., NADH dehydrogenase (complex I), cytochrome c oxidase (complex IV), and oxidative stress-sensitive aconitase was also detected following treatment with formaldehyde. Furthermore, formaldehyde caused a concentration-dependent increase in nuclear fragmentation and in the activities of the apoptosis-initiator caspase-9 and apoptosis-effector caspase-3/-7, indicating apoptosis progression. Our data suggests that formaldehyde exerts strong cytotoxicity, at least in part, by inducing oxidative stress, mitochondrial dysfunction, and eventually apoptosis. Changes in mitochondrial respiratory function and oxidative stress by formaldehyde may therefore be critical in methanol-induced toxicity.

Urokinase, urokinase receptor, and plasminogen activator inhibitor-1 expression on podocytes in immunoglobulin A glomerulonephritis.

BACKGROUND/AIMS: The purpose of this study was to investigate the expression of urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), and plasminogen activator inhibitor (PAI)-1 on podocytes in immunoglobulin A (IgA) glomerulonephritis (GN). METHODS: Renal biopsy specimens from 52 IgA GN patients were deparaffinized and subjected to immunohistochemical staining for uPA, PAI-1, and uPAR. The biopsies were classified into three groups according to the expression of uPA and uPAR on podocytes: uPA, uPAR, and a negative group. The prevalences of the variables of the Oxford classification for IgA GN were compared among the groups. RESULTS: On podocytes, uPA was positive in 11 cases and uPAR was positive in 38 cases; by contrast, PAI-1 was negative in all cases. Expression of both uPA and uPAR on podocytes was less frequently accompanied by tubulointerstitial fibrosis. CONCLUSIONS: Our results suggest a possible protective effect of podocyte uPA/uPAR expression against interstitial fibrosis.

Reanalysis of membranoproliferative glomerulonephritis patients according to the new classification: a multicenter study.

BACKGROUND: All types of membranoproliferative glomerulonephritis (MPGN) are progressive diseases with poor prognoses. Recently, a newly proposed classification of these diseases separated them into immune complex- and complement-mediated diseases. We investigated the frequency of C3 glomerulonephritis among previously diagnosed MPGN patients. METHODS: We conducted a retrospective study of patients diagnosed with MPGN at three tertiary care institutions between 2001 and 2010. We investigated the incidence of complement-mediated disease among patients diagnosed with MPGN. Progressive renal dysfunction was defined as a 50% reduction in the glomerular filtration rate or the need for renal replacement therapy. RESULTS: Among the 3,294 renal biopsy patients, 77 (2.3%) were diagnosed with MPGN; 31 cases were excluded, of which seven were diagnosed with systemic lupus nephritis, and the others were not followed for a minimum of 12 months after biopsy. Based on the new classification, complement-mediated MPGN was diagnosed in two patients (4.3%); only one patient developed progressive renal dysfunction. Among the immune complex-mediated MPGN patients, 17 patients developed progressive renal dysfunction. Serum albumin and creatinine levels at the time of MPGN diagnosis were risk factors of renal deterioration, after adjusting for low C3 levels and nephrotic syndrome. CONCLUSION: Complement-mediated glomerulonephritis was present in 4.3% of patients previously diagnosed with MPGN.

Indoxyl sulfate promotes apoptosis in cultured osteoblast cells.

BACKGROUND: Indoxyl sulfate (IS), an organic anion uremic toxin, promotes the progression of renal dysfunction. Some studies have suggested that IS inhibits osteoclast differentiation and suppresses parathyroid hormone (PTH)-stimulated intracellular cAMP production, decreases PTH receptor expression, and induces oxidative stress in primary mouse calvaria osteoblast cell culture. However, the direct effects of IS on osteoblast apoptosis have not been fully evaluated. Hence, we investigated whether IS acts as a bone toxin by studying whether IS induces apoptosis and inhibits differentiation in the cultured osteoblast cell line MC3T3-E1. METHODS: We assessed the direct effect of IS on osteoblast differentiation and apoptosis in the MC3T3-E1 cell line. We examined caspase-3/7 activity, apoptosis-related proteins, free radical production, alkaline phosphatase activity, and mRNA expression of type 1 collagen and osteonectin. Furthermore, we investigated the uptake of IS via organic anion transport (OAT). RESULTS: We found that IS increased caspase activity and induced apoptosis. Production of free radicals increased depending on the concentration of IS. Furthermore, IS inhibited the expression of mRNA type 1 collagen and osteonectin and alkaline phosphatase activity. The expression of OAT, which is known to mediate the cellular uptake of IS, was detected in in the MC3T3-E1 cell line. The inhibition of OAT improved cell viability and suppressed the production of reactive oxygen species. These results suggest that IS is transported in MC3T3-E1 cells via OAT, which causes oxidative stress to inhibit osteoblast differentiation. CONCLUSIONS: IS acts as a bone toxin by inhibiting osteoblast differentiation and inducing apoptosis.

The dose of cyclophosphamide for treating paraquat-induced rat lung injury.

BACKGROUND/AIMS: Cyclophosphamide (CP) is a promising treatment for severe cases of paraquat (PQ) poisoning. We investigated the effective dose of CP for mitigating PQ-induced lung injury. METHODS: Adult male Sprague-Dawley rats were allocated into five groups: control, PQ (35 mg/kg, intraperitoneal injection), and PQ + CP (1.5, 15, or 30 mg/kg). The dimensions of lung lesions were determined using X-ray microtomography (micro-CT), and histological changes and cytokine levels were recorded. RESULTS: The micro-CT results showed that 15 mg/kg CP was more effective than 1.5 mg/kg CP for treating PQ-induced lung injury. At a dose of 1.5 mg/kg, CP alleviated the histological evidence of inflammation and altered superoxide dismutase activity. Using 15 mg/kg CP reduced the elevated catalase activity and serum transforming growth factor (TGF)-ß1 level. CONCLUSIONS: A CP dose of > 15 mg/kg is effective for reducing the severity of PQ-induced lung injury as determined by histological and micro-CT tissue examination, possibly by modulating antioxidant enzyme and TGF-ß1 levels.

Quercetin reduces oxidative damage induced by paraquat via modulating expression of antioxidant genes in A549 cells.

Oxidative injury can occur in the lung through the generation of reactive oxygen species (ROS) via redox cycling owing to intentional or accidental ingestion of paraquat (PQ), a common herbicide. A wide array of phytochemicals has been shown to reduce cellular oxidative damage by modulating cytoprotective genes. Quercetin, a well-known flavonoid, has been reported to display cytoprotective effects by up-regulating certain cytoprotective genes. In this context, we investigated the effect of quercetin on PQ-induced cytotoxicity in alveolar A549 cells, modulation of antioxidant genes, activation of transcription factor-Nrf2 and its target HO-1 expression. Quercetin reduced PQ-induced cytotoxicity in A549 cells that was evaluated by both 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays. Modulation of antioxidant genes was compared when cells were treated with PQ, quercetin and both using qRT-PCR. Activation of transcription factor-Nrf2 and induction of its target gene, HO-1 was demonstrated by western blot analysis. A remarkable reduction in the ROS level as well as an increase in the total cellular glutathione (GSH) level occurred when PQ-exposed cells were treated with quercetin. Our findings suggest that quercetin may be used to mitigate or minimize oxidative stress via reducing the generation of ROS.

Mixtures of glyphosate and surfactant TN20 accelerate cell death via mitochondrial damage-induced apoptosis and necrosis.

Glyphosate, a common herbicide, is not toxic under normal exposure circumstances. However, this chemical, when combined with a surfactant, is cytotoxic. In this study, the mechanism of the additive effect of glyphosate and TN-20, a common surfactant in glyphosate herbicides, was investigated. After exposure of rat H9c2 cells to glyphosate and TN-20 mixtures, following assays were performed: flow cytometry to determine the proportion of cells that underwent apoptosis and necrosis; western blotting to determine expression of mitochondrial proteins (Bcl-2 and Bax); immunological methods to evaluate translocation of cytochrome C; luminometric measurements to determine activity of caspases 3/7 and 9; and tetramethyl rhodamine methyl ester assay to measure mitochondrial membrane potentials. Bcl-1 intensity decreased while Bax intensity increased with exposure to increasing TN-20 and/or glyphosate concentrations. Caspase activity increased and mitochondrial membrane potential decreased only when the cells were exposed to a mixture of both TN-20 and glyphosate, but not after exposure to either one of these compounds. The results support the possibility that mixtures of glyphosate and TN-20 aggravate mitochondrial damage and induce apoptosis and necrosis. Throughout this process, TN-20 seems to disrupt the integrity of the cellular barrier to glyphosate uptake, promoting glyphosate-mediated toxicity.

A case of scrub typhus requiring maintenance hemodialysis.

Renal failure caused by scrub typhus is known to be reversible. In most cases, renal function is almost fully restored after appropriate antibiotic treatment. A 71-year-old man was diagnosed with scrub typhus complicated by renal failure. A renal biopsy revealed histopathologic findings consistent with acute tubulointerstitial nephritis. Renal function did not improve 18 months after discharge and the patient required continuous hemodialysis. Although severe renal failure requiring dialysis is a rare complication of scrub typhus, we describe a case of scrub typhus requiring maintenance hemodialysis. To the best of our knowledge, this is the first such report.

Hyperuricemia as a marker for progression of immunoglobulin A nephropathy.

BACKGROUND: The variable clinical and histopathological manifestations of immunoglobulin A nephropathy (IgAN) make it difficult to predict disease progression. A recent study showed that hyperuricemia, a condition common in hypertension and vascular disease, may contribute to renal dysfunction and histological changes including renal arteriosclerosis, tubular atrophy, and interstitial fibrosis. Herein, we investigated the clinical significance of uric acid level at the time of biopsy, as a marker of IgAN progression. METHODS: We included 193 patients with biopsy-proven IgAN. Renal disease progression was defined as serum creatinine elevation above 1.2 mg/dL or over 20% elevation from baseline. Hyperuricemia was defined as a serum uric acid level ≥7.3 mg/dL in men and ≥5.3 mg/dL in women, which were 1 standard deviation above the mean value in the normal subjects. RESULTS: The hyperuricemia group (n=50) had higher blood pressure, body mass index, and serum creatinine, and a greater amount of proteinuria and a lower glomerular filtration rate than the nonhyperuricemia group (n=143). Hyperuricemia increased the risk of IgAN progression (odds ratio, 4.53; 95% confidence interval, 1.31-15.66). The disease progression group (n=26) had a greater frequency of hyperuricemia, hypertension, and nephrotic range proteinuria than the nonprogression group (n=119). The renal survival analysis showed that the hyperuricemia group had a higher rate of IgAN disease progression. CONCLUSION: Hyperuricemia at the time of diagnosis is an important marker for IgAN progression.

Effect of glutathione on the cadmium chelation of EDTA in a patient with cadmium intoxication.

In order to evaluate the efficiency and renal protective effects of glutathione during Ca(++)-EDTA chelation therapy for chronic cadmium intoxication, we measured the renal excretion of cadmium, ß(2)-microglobulin, proteinuria, and hematuria during intravenous administration of glutathione with Ca(++)-EDTA in a 54-year-old patient with chronic cadmium intoxication. We administered 500 mg of Ca(++)-EDTA and 50 mg/kg of glutathione alone or in 1 L of normal saline over the next 24 hours and repeated this over 12 consecutive days. During the first 3 days, the basal levels (only saline administration) were determined; during the second 3 days, Ca(++)-EDTA only was administered, for the third sequence of 3 days, Ca(++)-EDTA with glutathione was provided, and for the last 3 days, glutathione alone was given. One month later, the same protocol was repeated. There were six blood and urine samples to analyze in each group. The blood cadmium level was higher when the EDTA was infused together with glutathione (7.44 ± 0.73 µg/L, p < 0.01) compared to the basal level of 4.6 ± 0.44 µg/L. Also, the renal cadmium excretion was significantly higher in the EDTA with glutathione group than in the basal group (23.4 ± 15.81 µg/g creatinine vs 89.23 ± 58.52 µg/g creatinine, p < 0.01). There was no difference in the protein/creatinine and ß(2)-microglobulin/creatinine ratio in the urine (p > 0.05) among the groups. Furthermore, microhematuria and proteinuria did not develop over the observation period of 6 months. These results suggest that glutathione administration with EDTA might be an effective treatment modality for patients with cadmium intoxication.

Effect of glutathione administration on serum levels of reactive oxygen metabolites in patients with paraquat intoxication: a pilot study.

BACKGROUND/AIMS: Based on preliminary in vitro data from a previous study, we proposed that 50 mg/kg glutathione (GSH) would be adequate for suppressing reactive oxygen species in patients with acute paraquat (PQ) intoxication. METHODS: Serum levels of reactive oxygen metabolites (ROM) were measured before and after the administration of 50 mg/kg GSH to each of five patients with acute PQ intoxication. RESULTS: In one patient, extremely high pretreatment ROM levels began to decrease prior to GSH administration. However, in the remaining four cases, ROM levels did not change significantly prior to GSH administration. ROM levels decreased significantly after GSH administration in all cases. In two cases, ROM levels decreased below that observed in the general population; one of these patients died after a cardiac arrest at 3 hours after PQ ingestion, while the other represented the sole survivor of PQ intoxication observed in this study. In the survivor, ROM levels decreased during the first 8 hours of GSH treatment, and finally dropped below the mean ROM level observed in the general population. CONCLUSIONS: Treatment with 50 mg/kg GSH significantly suppressed serum ROM levels in PQ-intoxicated patients. However, this dose was not sufficient to suppress ROM levels when the PQ concentration was extremely high.

Effect of 835 MHz radiofrequency radiation exposure on calcium binding proteins in the hippocampus of the mouse brain.

Worldwide expansion of mobile phones and electromagnetic field (EMF) exposure has raised question of their possible biological effects on the brain and nervous system. Radiofrequency (RF) radiation might alter intracellular signaling pathways through changes in calcium (Ca(2+)) permeability across cell membranes. Changes in the expression of calcium binding proteins (CaBP) like calbindin D28-k (CB) and calretinin (CR) could indicate impaired Ca(2+)homeostasis due to EMF exposure. CB and CR expression were measured with immunohistochemistry in the hippocampus of mice after EMF exposure at 835 MHz for different exposure times and absorption rates, 1 h/day for 5 days at a specific absorption rate (SAR)=1.6 W/kg, 1 h/day for 5 days at SAR=4.0 W/kg, 5 h/day for 1 day at SAR=1.6 W/kg, 5 h/day for 1 day at SAR=4.0 W/kg, daily exposure for 1 month at SAR=1.6 W/kg. Body weights did not change significantly. CB immunoreactivity (IR) displayed moderate staining of cells in the cornu ammonis (CA) areas and prominently stained granule cells. CR IR revealed prominently stained pyramidal cells with dendrites running perpendicularly in the CA area. Exposure for 1 month produced almost complete loss of pyramidal cells in the CA1 area. CaBP differences could cause changes in cellular Ca(2+)levels, which could have deleterious effect on normal hippocampal functions concerned with neuronal connectivity and integration.

Clinical implication of urinary neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 in patients with acute paraquat intoxication.

BACKGROUND: Paraquat (PQ)-induced acute kidney injury (AKI) might show the role for reactive oxygen species (ROS) in AKI. The purpose of this study was to investigate the characteristics of early urinary biomarkers in patients with acute PQ poisoning. We prospectively investigated changes in urinary kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) in acute PQ intoxication. METHODS: From May 2008 to September 2008, 20 patients were included. Urine KIM-1, NGAL, and 8-hydroxy-2-deoxyguanosine (8-OH-dG) were measured at 6, 12, 24, 48, 72, and 120 h after ingestion. The serum creatinine was measured also at the same intervals. RESULTS: AKI was diagnosed in 11 out of 20 patients. There was a significant difference in the creatinine at 12 h between patients with AKI and those without AKI (0.50 +/- 0.15 vs. 1.04 +/- 0.53 mg/dL, p = 0.01). Urinary NGAL was higher in patients with AKI compared to patients without AKI at 24 h (2.84 vs. 0.96 ng/mL). Urinary KIM-1 was not different in comparisons between patients with AKI and those without AKI. Regardless of the AKI, the NGAL and KIM-1 were increased at between 24 and 48 h. CONCLUSION: PQ is a very potent stimulant of NGAL-1 and KIM-1. Therefore, the NGAL might reflect reactive oxygen species-induced kidney injury.

The area of ground glass opacities of the lungs as a predictive factor in acute paraquat intoxication.

Even though plasma paraquat (PQ) levels have known to be an informative predictor, many patients succumb at low PQ levels in acute PQ intoxication. This study was designed to see whether the high resolution computerized tomography (HRCT) of the lungs would be a predictive measure in acute PQ intoxication. HRCT of the lungs was obtained from 119 patients with acute PQ intoxication on 7 days after PQ ingestion. The areas with ground glass opacities (GGOs) were evaluated at five levels with the area measurement tool of the picture archiving and communication systems. Among 119 patients, 102 survived and 17 died. The plasma PQ levels were significantly higher in the non-survivors than in the survivors (2.6+/-4.0 microg/mL vs. 0.2+/-0.4 microg/mL, P=0.02). The area with GGOs was 2.0+/-6.4% in the survivors and 73.0+/- 29.9% in the non-survivors (P<0.001). No patients survived when the area with GGOs was more than 40% but all of the patients survived when the area affected by GGOs was less than 20%. In conclusion, the area of GGOs is a useful predictor of survival in acute PQ intoxication, especially in patients with low plasma PQ levels.

Marked recovery from paraquat-induced lung injury during long-term follow-up.

BACKGROUND/AIMS: Paraquat-induced lung injury has been considered a progressive and irreversible disease. The purpose of this study was to report the long-term evolution of lung lesions in eight survivors with significant paraquat-induced lung injuries who could be followed-up for longer than 6 months. METHODS: We retrospectively examined high-resolution computed tomography and pulmonary function test of eight survivors with significant paraquat-induced lung injurys. RESULTS: High-resolution computed tomography revealed a predominant pattern of irregularly shaped consolidation with traction bronchiectasis at 1-2 months after paraquat poisoning, a mixed pattern of irregularly shaped consolidation and ground-glass opacity at 3-12 months, and a mixed pattern of consolidation, ground-glass opacity, and honeycombing at 1-2 years. At 3-12 months after paraquat ingestion, the areas of consolidation had markedly decreased and the decreased lung volume had returned to normal. At 1-2 years after paraquat poisoning, the cystic changes had disappeared. At 2-3 years after paraquat poisoning, the decrease in forced vital capacity had greatly improved to the normal range. CONCLUSIONS: Recovery of nearly normal pulmonary structure and function may occur over several years following paraquat poisoning. Pulmonary function (both forced vital capacity and forced expiratory volume in 1 sec) evolved toward normal in the long-term survivors of paraquat poisoning with initial prominent lung injuries.

Benzene and toluene concentrations in a hemodialysis room in a medium sized South Korean city.

BACKGROUND/AIMS: The current study was designed to determine whether the indoor air pollution in a hemodialysis room (HD) was different from that of other comparable areas in a hospital. METHODS: Five air monitor samplers were hung on the ceiling and placed on the table in both the HD and general ward nursing stations, respectively. In addition, five samplers were placed in the nurse's breathing zone of the HD and the general ward, respectively. Ten air monitor samplers were also placed on the edge of the bed in the HD, which represented the patient's breathing zone. The levels of benzene and toluene were analyzed by GC/MS. RESULTS: In the general ward, the toluene concentration was significantly higher in the nurse breathing zone than that for the ceiling or table samples (p=0.001). The benzene concentration was also significantly higher in the general ward nurse breathing zone than that in the HD (p=0.006). In addition, the benzene concentrations on the table were higher at the general ward as compared to the HD (p=0.028), but there was no significant difference between the ceiling, general ward station and HD. CONCLUSIONS: Both the benzene and toluene concentrations in the HD appear to be more affected by the outdoor atmospheric conditions than by any potential indoor internal sources.