• Title/Summary/Keyword: pulmonary toxicity

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Comprehensive Review of Acute Respiratory Failure Following Inhalation Exposure to Waterproofing Agents (방수 스프레이 흡입 노출로 인한 급성 호흡기 중독 사례 및 원인 고찰)

  • Park, Donguk;Choi, Yeyong
    • Journal of Environmental Health Sciences
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    • v.38 no.6
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    • pp.451-459
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    • 2012
  • Background: In Korea, a healthy 36-year-old man developed acute interstitial pneumonitis soon after inhaling a waterproofing spray which he had applied at home to his outdoor jacket. Objectives: The objectives of this study were to review cases of varying degrees of respiratory toxicity and poisoning in connection with the use of waterproofing spray and summarize major reasons for cases of poisoning. Methods: We searched articles reporting on a combination of a waterproofing agent and/or respiratory symptoms, including acute respiratory syndrome, lung injury, pneumonia, pulmonary toxicity, and respiratory disease. Results: We reviewed a number of cases of varying degrees of respiratory toxicity and poisoning resulting from inhalation of waterproofing spray containing fluorocarbon co-polymer, solvents and propellants reported in a variety of countries. The literature searches concluded that among the ingredients of waterproofing agents, fluorinated polymer may cause acute respiratory health effects. Conclusion: Environmental policy should be implemented in order to prevent consumers from using household and industrial products including waterproofing agents. In addition, a national surveillance system should be created to collect cases of poisoning caused by the use of consumer products.

Nasal and Pulmonary Toxicity of Titanium Dioxide Nanoparticles in Rats

  • Kwon, Soonjin;Yang, Young-Su;Yang, Hyo-Seon;Lee, Jinsoo;Kang, Min-Sung;Lee, Byoung-Seok;Lee, Kyuhong;Song, Chang-Woo
    • Toxicological Research
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    • v.28 no.4
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    • pp.217-224
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    • 2012
  • In recent decades, titanium dioxide ($TiO_2$) nanoparticles have been used in various applications, including paints, coatings, and food. However, data are lacking on the toxicological aspects associated with their use. The aim of this study was to assess the inhalation toxicity of $TiO_2$ nanoparticles in rats by using inhalation exposure. Male Wistar rats were exposed to $TiO_2$ nanoparticles for 2 weeks (6 hr/day, 5 days/week) at a mean mass concentration of $11.39{\pm}0.31mg/m^3$. We performed time-course necropsies at 1, 7, and 15 days after exposure. Lung inflammation and injury were assessed on the basis of the total and individual cell counts in bronchoalveolar lavage fluid (BALF), and by biochemical assays, including an assay for lactate dehydrogenase (LDH). Furthermore, histopathological examination was performed to investigate the lungs and nasal cavity of rats. There were no statistically significant changes in the number of BALF cells, results of biochemical assays of BALF and serum, and results of cytokine analysis. However, we did observe histopathological changes in the nasal cavity tissue. Lesions were observed at post-exposure days 1 and 7, which resolved at post-exposure day 15. We also calculated the actual amounts of $TiO_2$ nanoparticles inhaled by the rats. The results showed that the degree of toxicity induced by $TiO_2$ nanoparticles correlated with the delivered quantities. In particular, exposure to small particles with a size of approximately 20 nm resulted in toxicity, even if the total particle number was relatively low.

Identification and Characterization of Genes that are Induced after Cadmium Exposure

  • Lee, Mi-Ock
    • Proceedings of the PSK Conference
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    • 2003.10a
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    • pp.73-73
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    • 2003
  • The heavy metal cadmium is a xenobiotic toxicant of environmental and occupational concern and it has been classified as a human carcinogen. Inhalation of cadmium has been implicated in the development of emphysema and pulmonary fibrosis, but, the detailed mechanism by which cadmium induces adverse biological effects is not yet known. Therefore, we undertook the investigation of genes that are induced after cadmium exposure to illustrate the mechanism of cadmium toxicity. (omitted)

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Effects of Nitrofurantoin on Lipid Peroxidation and Reactive Oxygen Radical Generation in Porcine Lung Microsome (Nitrofurantion이 폐장 미크로솜 지질과산화와 반응성 산소 라디칼 생성에 미치는 영향)

  • Paick, Jae-Seung;Kim, Si-Whang;Kim, Hae-Won;Chung, Myung-Hee;Kim, Myung-Suk
    • The Korean Journal of Pharmacology
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    • v.21 no.1
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    • pp.34-48
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    • 1985
  • In vitro effects of nitrofurantoin, an antimicrobial agent for acute and chronic urinary tract infection, on the lung microsomal lipid peroxidation and the generation of reactive oxygen radicals were investigated to elucidate the biochemical mechanisms of its in vivopulmonary toxicity. The interaction of nitrofurantoin with porcine lung microsome resulted in significant lipid peroxidation. In addition, nitrofurantoin stimulated the generation of reactive oxygen radicals, $O^{-}_{2}{\cdot},\;H_2O_2$ as well as a highly reactive secondary oxygen species, $OH{\cdot}$. The stimulation of lipid peroxidation was inhibited not only by superoxide dismutase and catalase, but also by hydroxyl radical scavengers, mannitol and thiourea. Neither singlet oxygen $({^1}O_{2})$ was detected during the incubation of microsome with nitrofurantoin, nor lipid peroxidation was inhibited by singlet oxygen scavengers. When incubated anaerobically under the nitrogen atmosphere, the ability of nitrofurantoin to stimulatle lipid peroxidation was abolished. It appears that NADPH-dependent metaboliam of nitrofurantoin in pulmonary microsome under aerobic condition is accompanied by the stimulation of lipid peroxidation through the mediation of reactive oxygen radicals, particularly hydroxyl radical. It is strongly suggested from these results that the stimulation of pulmonary microsomal lipid peroxidation by the reactive oxygen radical may be a in vivo mechanism of pulmonary toxicity caused by nitrofurantoin.

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Noninvasive Monitoring of Bleomycin-induced Lung Injury in Rats Using Pulmonary Function Test

  • Yang, Mi-Jin;Yang, Young-Su;Kim, Yong-Bum;Cho, Kyu-Hyuk;Heo, Jeong-Doo;Lee, Kyu-Hong;Song, Chang-Woo
    • Toxicological Research
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    • v.24 no.4
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    • pp.273-280
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    • 2008
  • The single intratracheal instillation (ITI) of bleomycin (BLM) is a widely used method for inducing experimental pulmonary fibrosis in rat model. In the present study, pulmonary function tests (PFTs) of tidal volume ($V_T$), minute volume ($V_M$), and respiratory frequency ($F_R$) have been applied to study their possibility as a tool to monitor the progress of BLM-induced lung injury in rat model. Rats were treated with a single ITI of BLM (2.5 mg/kg) or saline (control). Animals were euthanized at 3, 7, 14, 21, and 28 days post-ITI. Lung toxicity effects were evaluated by inflammatory cell count, lactate dehydrogenase (LDH) activity in the bronchoalveolar lavage fluid (BALF), and light microscopic examination of lung injury. The PFT parameters were measured immediately before the animals were sacrificed. BLM treatment induced significant cellular changes in BALF-increase in number of total cells, neutrophils, and lymphocytes along with sustained increase in number of macrophages compared to the controls at days 3, 7, and 14. BALF LDH level was significantly increased compared to that in the controls up to day 14. On day 3, infiltration of neutrophils was observed in the alveolar spaces. These changes developed into marked peribronchiolar and interstitial infiltration by inflammatory cells, and extensive thickening of the interalveolar septa on day 7. At 14, 21, and 28 days, mild peribronchiolar fibrosis was observed along with inflammatory cell infiltration. The results of PFT show significant consistencies compared to the results of other toxicity tests. These data demonstrate that the most suitable time point for assessing lung fibrosis in this model is 14 days post-ITI of BLM based on the observation of fibrosis at 14, 21, and 28 days. Further, the progress of lung injury can be traced by monitoring the PFT parameters of $F_R$, $V_T$, and $V_M$.

The current status of fumonisin toxicosis in domestic animals: A review (가축의 fumonisin 중독증에 대한 최근 연구 동향 : 종설)

  • Lim, Chae-woong;Rim, Byung-moo
    • Korean Journal of Veterinary Research
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    • v.35 no.2
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    • pp.405-416
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    • 1995
  • FBs, secondary metabolites of several species of Fusaria, especially Fusarium moniliforme and F proliferatum, are commonly contaminated in com and other food grains throughout the world. Only recently identified, these mycotoxins have been associated field outbreaks of ELEM in horses and PPE in pigs. Currently, naturally or experimentally induced FB toxicosis has been studied in poultry, ruminants and rabbits. Poultry fed FB showed decreased growth rate, performance, and immune competence, as well as embryopathic, and embryocidal effects, and ricktes. Ruminants seem to be relatively less susceptible to FBs than other doestic animal. FB toxicosis reveals that liver is a target organ in all species, although other organs are affected in a species specific manner. Recently, the main target organs for $FB_1$ toxicity in rabbits was shown to be the kidney. Even low concentrations of FBs are likely to be a problem for animal health. A current study being conducted showed that feed containing low level of $FB_1$ reduces the ability of pulmonary intravascular macrophages in pig to clear blood-borne particles which would increase the susceptibility of animals to bacterial disease. The mechanism of FB toxicity remains unknown, but may be related to altered sphingolipid biosynthesis by inhibiting sphinganine N-acyltransferase. Elevations of serum and tissue SA:SO ratio have been observed in horse, pig, chicken, turkey, and rabbit, which could could serve as in effective biomarker for consumption of FB-containing feeds. There is limited information detailing dose-effect relationships either from field cases or in the laboratory. More research on the factors, including the prevalence and tolerance levels of FBs in feedstuffs that cause domestic animal disease associated with FBs, is urgently needed.

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Effects of Methanol Extract from Terminalia chebulae on Renal and Pulmonary Toxicities Induced by Paraquat in Rats (가자(Terminalia chebulae) 메탄올 추출물이 paraquat 독성에 의한 흰 쥐의 신장 및 폐조직에 미치는 영향)

  • Park, Jong-Ok
    • Journal of Life Science
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    • v.18 no.1
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    • pp.129-135
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    • 2008
  • Paraquat (1,1-dimethyl 4,4' -dipyridium dichloride; PQ) is a kind of herbicide. Terminalia chebulae (TC) has been used as a medicine in China and in Korea for treating illnesses such as diarrhea, collapsed anus, spasmodic, diphtheria, asthma etc.. This study was to examin new physiological activities of methanol extract of TC (TCM) on the toxicity of PQ. It was observed biochemical effects on the toxicity of PQ in kidney and lung tissues after treatment orally administered 100, 200, 300 mg/kg of TCM daily for two weeks. In the experiment related to the toxicity of PQ, we got following results: renal and pulmonary lipid peroxide contents, activities of aminopyrine N-demethylase, aldehyde oxidase and xanthine oxidase were significantly increased in control group as compared with normal group, in the treatment of TCM the values were decreased as compared with control group. Activities of superoxide dismutase, catalase and glutathione peroxidase which are free radical scavenging enzymes were also increased in control group as compared with normal goup, but were decreased in TCM group as compared with control group. Collagen content and glucose-6-phosphatase activity in lung tissue were increased in control group as compared with normal, but was decreased in TCM group as compared with control group. From these results, we concluded that TCM can playa role as an effective agent to decrease toxicity of PQ.

A Case of Severe Bleomycin-Induced Pneumonitis at Non-Hodgkin's Lymphoma (비호즈킨 림프종 환자에서 저용량의 Bleomycin에 의해 발생한 급성 중증 폐독성 1예)

  • Han, Dong-Ha;Min, Young-Joo;Yoon, Je-Hyun;Park, Jong-Ho;Ahn, Jong-Joon;Lee, Ki-Man;Park, Jae-Hoo
    • Tuberculosis and Respiratory Diseases
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    • v.52 no.3
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    • pp.260-264
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    • 2002
  • Bleomycin-induced pulmonary toxicity usually occurs in the elderly patients (greater than 70 years old), patients with a cumulative dose above 400 units, previous chest radiotherapy, oxygen therapy, and renal failure. However, there are some reports of severe pneumonitis that developed after administering low bleomycin doses(less than 100 units). In severe bleomycin-induced pneumonitis in non-Hodgkin's lymphoma patients, the response to corticosteroid is poor and the mortality rate is very high, approximately 83%. Therefore, clinicians should have a low threshold for investigating and treating bleomycin-induced pneumonitis. Here, we report a case of severe bleomycin-induced pneumonitis as a complication of a non-Hodgkin's lymphoma treatment.

Effect of Fiber Number Per Mass Concentration in Korean Produced Asbestos on Lung Function and Pathology (중량당 섬유수가 다른 국내산 석면이 폐 기능과 폐 조직에 미치는 영향 평가)

  • Chung, Yong Hyun;Han, Jeong Hee;Kang, Min Gu;Kim, Jong Kyu;Yang, Jeong Sun
    • Journal of Korean Society of Occupational and Environmental Hygiene
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    • v.22 no.4
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    • pp.301-308
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    • 2012
  • Objectives: To evaluate the pulmonary toxicity of 2 Korea asbestos(chrysotile, anthophyllite), Sprague-Dawely rats were exposed to 2 mg domestic asbestos by intratracheal instillation(IT). Methods: Lung function of rats was analyzed by pressure transducer(MAX1320, Buxco Electronics, USA). The effects of 2 mg asbestos(chrysotile ; $8,814,244{\times}10^{6}$ fibers/mg, average diameter 0.08 ${\mu}m$, average length 4.39 ${\mu}m$, anthophyllite ; $5,182{\times}10^{6}$ fibers/mg, average diameter 0.95 ${\mu}m$, average length 7.29 ${\mu}m$) on pulmonary function and pathological changes were evaluated at after a single IT. Lung function and histopathological evaluation were assessed in 5 animals from each group at each time point. Results: Due to differences in fiber numbers, chrysotile induce marked lung pathology and lung function change than anthophyllite at the same mass dose. Chrysotile showed notable thickening of interstitial areas surrounding the alveolar ducts and terminal bronchioles. Conclusions: On a mass dose basis, chrysotile that have 1,700 times numbers of fibers per unit weight than anthophyllite produced a greater persistent lung injury than anthophllite for at least 4 weeks after exposure.

LJ-2698, an Adenosine A3 Receptor Antagonist, Alleviates Elastase-Induced Pulmonary Emphysema in Mice

  • Boo, Hye-Jin;Park, So Jung;Noh, Myungkyung;Min, Hye-Young;Jeong, Lak Shin;Lee, Ho-Young
    • Biomolecules & Therapeutics
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    • v.28 no.3
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    • pp.250-258
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    • 2020
  • Emphysema, a major component of chronic obstructive pulmonary disease (COPD), is a leading cause of human death worldwide. The progressive deterioration of lung function that occurs in the disease is caused by chronic inflammation of the airway and destruction of the lung parenchyma. Despite the main impact of inflammation on the pathogenesis of emphysema, current therapeutic regimens mainly offer symptomatic relief and preservation of lung function with little therapeutic impact. In the present study, we aimed to discover novel therapeutics that suppress the pathogenesis of emphysema. Here, we show that LJ-2698, a novel and highly selective antagonist of the adenosine A3 receptor, a G protein-coupled receptor involved in various inflammatory diseases, significantly reversed the elastase-induced destructive changes in murine lungs. We found that LJ-2698 significantly prevented elastase-induced airspace enlargement, resulting in restoration of pulmonary function without causing any obvious changes in body weight in mice. LJ-2698 was found to inhibit matrix metalloproteinase activity and pulmonary cell apoptosis in the murine lung. LJ-2698 treatment induced increases in anti-inflammatory cytokines in macrophages at doses that displayed no significant cytotoxicity in normal cell lines derived from various organs. Treatment with LJ-2698 significantly increased the number of anti-inflammatory M2 macrophages in the lungs. These results implicate the adenosine A3 receptor in the pathogenesis of emphysema. Our findings also demonstrate the potential of LJ-2698 as a novel therapeutic/preventive agent in suppressing disease development with limited toxicity.