• 제목/요약/키워드: inhalation toxicity

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Synthesis, Characterization and Identification of In Vitro and In Vivo DNA adducts of 1- and 2-Bromopropane

  • Moon, Yoon-Soo;Basnet, Arjun;Zhao, Long-Xuan;Kim, Eun-Kyung;Lim, Hyun-Tae;Chae, Whi-Gun;Jeong, Tae-Cheon;Lee, Eung-Seok
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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    • pp.246.2-247
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    • 2003
  • It has been reported that 2-bromopropane might be a causative agent for reproductive toxicity and have immunotoxic effects. 1-Bromopropane known as an alternative to ozone depleting solvents, which has structural similarity to 2-bromopropane, has been reported to be neurotoxic to rats in long-term inhalation exposure. (omitted)

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Study on Inhalation Toxicity of Halogen Compound Using Rats

  • Kim, Hyeon-Yeong;Lim, Cheol-Hong;Chung, Yong-Hyun;Maeng, Seung-Hee;Lee, Sung-Bae;Han, Jeong-Hee;Jheon, Yoon-Seok;Lee, Yong-Mook
    • 한국환경독성학회:학술대회논문집
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    • 한국환경독성학회 2002년도 춘계학술대회(Genomics, Proteomics, and Risk Assesment):환경독성 및 위해성 평가 국제 심포지움
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    • pp.37-38
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    • 2002
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수은 체온계와 관련된 손상 및 중독에 대한 체계적 고찰 (A Systematic Review of Injury or Poisoning Related to Mercury Thermometer)

  • 이요섭;주영선;유제성;정성필;정현수;이한식
    • 대한임상독성학회지
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    • 제12권1호
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    • pp.22-30
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    • 2014
  • Purpose: The purpose of this systematic review was to evaluate the evidence regarding injury and poisoning associated with the clinical mercury thermometer. Methods: Electronic literature searches were conducted for identification of relevant studies and case reports of injury and poisoning associated with the clinical mercury thermometer. The search outcomes were limited to literature with English and Korean languages published from 1966. Studies related to occupational mercury exposure, or mercury exposure from sphygmomanometer, barometer, and fluorescent light were excluded. Results: A total of 60 reports, including 59 case reports, were finally included. Of those, nine cases pertained to an intact thermometer as a foreign body, 25 injuries were related to a thermometer, and 26 cases involved exposures to mercury from a broken thermometer. Case reports were classified according to severity into 16 mild, 41 moderate, and two severe cases. Two cases of mortality were reported, one was deliberate intravenous injection of mercury and the other was acute vapor inhalation of mercury from broken thermometers. Conclusion: Findings of this systematic review suggested that the mercury thermometer could cause various forms of poisoning and injury. In particular, inhalation of mercury vapor from a broken thermometer can lead to systemic toxicity requiring chelating therapy.

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SD흰쥐를 이용한 n-decane의 28일 반복흡입독성연구 (A Twenty-Eight Days Inhalation Toxicity Study of N-decane in Sprague Dawley Rats)

  • 임경택;김현영;송경석;정용현;장희경;한정희;이성배;전윤석;이용묵;유일재
    • Environmental Analysis Health and Toxicology
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    • 제19권4호
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    • pp.345-352
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    • 2004
  • N-decane은 지방족탄화수소로 다른 탄환수소들과 같이 혼합된 형태로 존재하며 페인트 제거제나 드라이 크리닝 제품에 사용된다. 최근의 본 연구팀이 실시한 전자산업계의 MSDS 신뢰성조사 결과에 따르면 세정제의 사용 경향은 과거의 방향족 탄화수소나 CFC. HCFC에서 $C_{10}$이상의 지방족탄화수소 물질로 변화되고 있는 경향을 보여주었다. Stoddard solvent나 나프타 같은 탄화수소 혼합물에 대한 작업 환경노출기준은 설정되어있지만 n-decane에 대해서는 제한적인 독성자료 밖에 없으며 작업환경노출기준은 설정되어 있지 않다. 따라서 작업환경에 대한 적절한 관리기준제시와 독성학적 자료를 제공하기 위해 n-decane을 28일 반복 흡입독성시험을 실시하였다. 6주령 흰쥐로 체중이 229$\pm$10g되는 숫컷과 165$\pm$7g되는 암컷 흰쥐를 4개 용량군 즉 대조군, 저농도군(50ppm), 중농도군(200ppm), 고농도군(800ppm) (각군당 10마리)으로 설정하여 하루 6시간, 주5일로 4주간 흡입쳄버에서 노출시켰다. 28일간 노출 후 n-decane의 노출용량에 따른 암수의 체중에는 유의한 변화가 없었으며 유의한 혈액학적 생화학적 변화도 발견되지 않았다. 고농도로 노출된 수컷 몇 마리에서 고환 세정관에서의 공포화(vacuolization)가 발견되었으나, 간신장, 비장, 폐, 부신, 심장, 뇌 등 다른 장기에 대한 조직병리학적 검사에서는 뚜렷한 조직병리학적인 변화를 발견할 수 없었다.

백서에서 흡인된 티타니아 나노입자의 생체 내 분포에 관한 연구 (Biodistribution of Inhaled Titania ($TiO_2$) Nanoparticles in Rats)

  • 최세훈;박계현;전상훈;김주현;정진행;조소혜;박종구;김태헌
    • 대한기관식도과학회지
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    • 제16권1호
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    • pp.33-38
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    • 2010
  • Titania nanomaterials are widely used as cosmetics and dyes, however the impacts on human health are uncertain, We investigated the biodistribution of inhaled titania nanoparticles in rats, Methods Eight weeks-old SD rats were intubated and inhaled with 3 mg titania nanoparticles, twice a week, for 2 weeks, After inhalation, the rats were sacrificed and tissues or heart, lung. intestine, brain, and liver were obtained, We investigated the tissues with optical microscope (OM), transmission electron microscope (EM), scanning EM, And to analyze titania concentration of each tissue, we lysed the tissues with radioimmunoprecipitation assay (RlPA) lysis buffer or acid. Results Granulation tissues in lung were confirmed on the optical microscope, however the other organs had no abnormalities in OM images, In EM images, the rats which inhaled titania nanoparticles showed calcium deposition at heart, brain, and intestine, Titania concentration in lung was increased on the inhaled rat sacrificed I month after last exposure. Conclusion Inhaled titania nanoparticles is thought to be deposited and make inflammatory reaction in lung, and the deposition was not efficiently cleared over a month. However inhaled titania nanoparticles may rarely pass through the alveolus-blood barrier and distribute to other organs of the bod.

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Differential Effects between Cigarette Total Particulate Matter and Cigarette Smoke Extract on Blood and Blood Vessel

  • Park, Jung-Min;Chang, Kyung-Hwa;Park, Kwang-Hoon;Choi, Seong-Jin;Lee, Kyuhong;Lee, Jin-Yong;Satoh, Masahiko;Song, Seong-Yu;Lee, Moo-Yeol
    • Toxicological Research
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    • 제32권4호
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    • pp.353-358
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    • 2016
  • The generation and collection of cigarette smoke (CS) is a prerequisite for any toxicology study on smoking, especially an in vitro CS exposure study. In this study, the effects on blood and vascular function were tested with two widely used CS preparations to compare the biological effects of CS with respect to the CS preparation used. CS was prepared in the form of total particulate matter (TPM), which is CS trapped in a Cambridge filter pad, and cigarette smoke extract (CSE), which is CS trapped in phosphate-buffered saline. TPM potentiated platelet reactivity to thrombin and thus increased aggregation at a concentration of $25{\sim}100{\mu}g/mL$, whereas 2.5~10% CSE decreased platelet aggregation by thrombin. Both TPM and CSE inhibited vascular contraction by phenylephrine at $50{\sim}100{\mu}g/mL$ and 10%, respectively. TPM inhibited acetylcholine-induced vasorelaxation at $10{\sim}100{\mu}g/mL$, but CSE exhibited a minimal effect on relaxation at the concentration that affects vasoconstriction. Neither TPM nor CSE induced hemolysis of erythrocytes or influenced plasma coagulation, as assessed by prothrombin time (PT) and activated partial thromboplastin time (aPTT). Taken together, CS affects platelet activity and deteriorates vasomotor functions in vitro. However, the effect on blood and blood vessels may vary depending on the CS preparation. Therefore, the results of experiments conducted with CS preparations should be interpreted with caution.

Ozone Inhalation with 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)- 1-butanone and/or Dibutyl Phthalate Induced Cell Cycle Alterations via Wild-type p53 Instability in B6C3F1 Mice

  • Kim, Min-Young;Song, Kyung-Suk;Park, Gun-Ho;Kim, Hyun-Woo;Park, Jin-Hong;Kim, Jun-Sung;Jin, Hwa;Kook-Jong, Eu;Cho, Hyun-Sun
    • Toxicological Research
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    • 제20권1호
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    • pp.71-82
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    • 2004
  • Changes in cell cycle control in the lungs and liver of the B6C3F1 mice (20 males per each group) exposed to ozone (0.5 ppm), 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK, 1.0 mg/kg), and dibutyl phthalate (DBP, 5,000 ppm) after 52 weeks were examined through Western, Northern blot, and immunohistochemistry based on alterations in protein expression levels of G1/S checkpoints (cyclin D1, cyclin E, and PCNA), G2/M checkpoints (cyclin B1, cyclin G, and cyclin A), negative regulators (p53, p21, GADD45, and p27), and positive regulator (mdm2). Expression levels of cyclins D1, E, G, PCNA, mutant p53, and mdm2 proteins were higher in the lungs and livers treated with combination of toxicants than in those treated with ozone only. Expression levels of the wild-type and mutant p53, p21, GADD45, p27, and mdm2 proteins and mRNAs were higher in toxicant-treated groups than those of the control. Immunohistochemical analysis revealed staining intensities of the PCNA, cyclin D1, c-myc and mdm2 protein- treated lungs and livers were stronger than those of the control group. Our results showed that combined treatment of ozone with NNK/DBP altered the cell cycle control through instability of the wild-type p53 gene. Such pivotal p53-mediated cell cycle alterations may be responsible for the toxicity observed under our experimental condition. These results may be applied to risk assessment of mixture-induced toxicity.

CMIT/MIT 가습기살균제 사용에 따른 피해구제 신청자의 노출등급 및 노출특성 분석 (Analysis of Exposure Characteristics and Exposure Rating of Participants with Injuries from CMIT/MIT Humidifier Disinfectants)

  • 민기홍;신정현;조은경;이슬아;신지훈;김동준;우재민;최윤형;양원호
    • 한국환경보건학회지
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    • 제49권3호
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    • pp.169-177
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    • 2023
  • Background: The Korea Centers for Disease Control and Prevention (KCDC) has identified cases of people suspected of suffering lung disease potentially caused by chloromethylisothiazolinone/methylisothiazolinone (CMIT/MIT) used in humidifier disinfectants (HDs). The Korean Ministry of Environment (MoE) epidemiological investigation and toxicity test study found that HDs caused health damage such as asthma and lung disease. Objectives: The main purposes of this study were to classify the HD exposure rating and to analyze the exposure characteristics that affect exposure to CMIT/MIT HDs. Methods: The exposure characteristics and socio-demographic characteristics of victim participants using CMIT/MIT HDs were investigated through questionnaires. An inhalation no observed adverse effect level (NOAEL) for CMIT/MIT was produced based on inhalation toxicity values. Exposure ratings (class 1~class 2) were cross-tabulated with clinical ratings (acceptable~unacceptable). A correlation analysis was conducted with the main exposure characteristics that affect the exposure concentration of CMIT/MIT HDs. Results: The concentration in indoor air of CMIT/MIT was 8.75±25.40 ㎍/m3, and the exposure concentration was 2.30±6.29 ㎍/m3. The CMIT/MIT exposure rating of 67 participants with high exposures of not more than MOE 100 were evaluated as 14.5%, while the damage participants who matched the clinical rating made up 4.5%. The exposure concentration of CMIT/MIT showed a positive correlation with the daily usage amount and usage frequency, and a negative correlation with volume of the indoor environment. Conclusions: A new exposure rating could be suggested and calculated based on the MOE, and the factors affecting the exposure concentration could be identified.

초오약침의 단회 및 4주 반복 투여 독성에 관한 실험적 연구 (An Experimental Study on Single-dose and 4 Weeks Repeated-dose Toxicity of Aconitum ciliare Decaisne Pharmacopuncture)

  • 이현수;이윤규;이봉효;김재수;임성철;이현종
    • Korean Journal of Acupuncture
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    • 제34권4호
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    • pp.241-250
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    • 2017
  • Objectives : This study was performed to examine the toxicity of Aconitum ciliare Decaisne pharmacopuncture(ADP). Methods : The toxicity was evaluated for lethal dose for 50 percent kill(LD50), single dose and repeated dose for 4 weeks. Toxic symptoms, weight measurement, hematological test, blood biochemical test, visual examination and weight measurement of major organs and histopathological test were observed for 4 weeks. Dose of 300, 600, 1,200, 2,400, 3,600, 4,800, 6,000, 7,200 mg/kg in the LD50 experiment, 300, 600, 1,200 mg/kg/day in the single experiment, 150, 300, 600 mg/kg/day in 4 weeks experiments were injected into BALB/c mice. The ADP was injected into ST36 of the right leg. Normal saline solution of same volume was used for control group. In 24 hours after the last treatment, blood samples were taken after anesthesia by inhalation of ethyl ether. After that, the BALB/c mice were euthanized. Their heart, lungs, kidneys, liver and reproductive organs were removed and weighed. Histopathological evaluation was also performed. Results : ADP's LD50 was measured at 6,000 mg/kg. In both single and repeated dose toxicity test, no BALB/c mouse died during the experiments. ADP treatment for 4 weeks did not show any significant changes in toxic symptoms, weight measurement, hematological test, blood biochemical test, visual examination and weight measurement of major organs and histopathological test. Conclusions : As a result, ADP's LD50 was 6,000 mg/kg and repeated dose at a concentration of 600 mg/kg or less is considered to be not harmful for clinical treatment.

Identification of Genes that are Induced after Cadmium Exposure by Suppression Subtractive Hybridization

  • 이미옥
    • 한국환경독성학회:학술대회논문집
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    • 한국환경독성학회 2003년도 춘계학술대회
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    • pp.107-107
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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 For this purpose, we employed the polymerase chain reaction-based suppression subtractive hybridization technique. We identified 29 different cadmium-inducible genes in human peripheral mononuclear cells, such as macrophage migration inhibitory factor, lysophosphatidic acid acyltransferase-${\alpha}$, enolase-1${\alpha}$, VEGF, Bax, neuron-derived orphan receptor-1, and Nur77, which are known to be associated with inflammation, cell survival, and apoptosis. Induction of these genes by cadmium treatment was further confirmed by semi-quantitative reverse-transcription polymerase chain reaction. Further, we found that these genes were also induced after cadmium exposure in normal human lung fibroblast cell line, WI-38, suggesting potential use of this induction profile to monitor cadmium toxicity in the lung. Next, Nur77, one of cadmium-inducible genes, was further studied since the products of Nur77 are known to be involved in the apoptotic process of lung cells. Following cadmium treatment, Nur77 gene expression was increased at protein-level in A549 cells. Consistently, the reporter containing Nur77 binding sequence was activated by 2.5-fold after exposure to cadmium in reporter gene analysis by transient transfection experiments. When the plasmid encoding dominant negative Nur77 that represses the transcriptional function of wild-type Nur77 was transfected into A549 cells, the expression of Bax was significantly reduced, suggesting that induction of Nur77 was an important process in cadmium-induced apoptosis in the cells. Cadmium induced the expression of Nur77 in vivo, confirming the relevance of the data obtained in viro. Together our results suggest that Nur77 gene expression in exposure to cadmium leads apoptosis of lung cells which may cause pathological changes in lung.

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