摘要:

Solid waste samples taken from the etching reactor, the turbo pump, and the waste air system of a plasma etching technology line in semiconductor production were studied as to their genotoxic properties in a bacterial repair test, in the Ames/Salmonella microsome assay, in the SOS chromotest, in primary mouse hepatocytes, and in Chinese hamster V79 cell cultures. All three waste samples were found to be active by inducing of unscheduled DNA‐synthesis in mouse hepatocytes in vitro. In the bacterial rec‐type repair test with Proteus mirabilis, waste samples taken from the turbo pump and the vacuum pipe system were not genotoxic. The waste sample taken from the chlorine‐mediated plasma reactor was clearly positive in the bacterial repair assay and in the SOS chromotest with Escherichia coli. Mutagenic activity was demonstrated for all samples in the presence and absence of S9 mix made from mouse liver homogenate. Again, highest mutagenic activity was recorded for the waste sample taken from the plasma reactor, while samples collected from the turbo pump and from the waste air system before dilution and liberation of the air were less mutagenic. For all samples chromosomal damage in V79 cells was not detected, indicating absence of clastogenic activity in vitro. Altogether, these results indicate generation of genotoxic and mutagenic products as a consequence of chlorine‐mediated plasma etching in the microelectronics industry and the presence of genotoxins even in places distant from the plasma reactor. Occupational exposure can be expected both from the precipitated wastes and from chemicals reaching the environment with the air stream.

ISSN:0098-4108    

DOI:10.1080/15287399309531754

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

One group of male, pathogen‐free, Fischer 344 rats was exposed to about 17‐fold diluted exhaust generated by an M85 methanol‐fueled engine (methanol with 15% gasoline) without catalyst for 8 h, and then the rates of recovery from the resulting increased levels of plasma formaldehyde and carboxyhemoglobin in their erythrocytes were measured. The carboxyhemoglobin level in the erythrocytes was restored within 4 h, whereas the plasma formaldehyde level was still elevated after 4 h but was restored to the normal level within 8 h. No methanol or formic acid was detected in the plasma. Another group of rats was exposed to the same dilution of exhaust for 8 h/d for 7 d, and then the recovery from histopathological damage of the nasal cavity and lungs was also examined. Hyperplasia/squamous metaplasia and erosion of the respiratory epithelium lining the nasoturbinate, maxilloturbinate, or nasal septum, and infiltration of neutrophils into the submucosa at level 1 (level of the posterior edge of the upper incisor teeth) were observed immediately after the exposure period. Lesions of the respiratory epithelium at level 2 (incisive papilla) were less than those at level 1. Slight lesions at levels 1 or 2 were still noticed 1 wk after exposure, but not 4 wk after exposure. Just after exposure, decreases of Clara cells in the terminal bronchiolus and of cilia in the bronchial/bronchi‐olar epithelium were also observed. Moreover, focal hypertrophy of alveolar walls and increase of macrophages were observed in parts adjacent to respiratory bronchiolus. One week after the exposure period, these changes were no longer seen. These results indicate that changes in the blood and in the nasal cavity and lungs caused by methanol‐fueled engine exhaust are reversible. However, complete recovery from damage of the nasal cavity caused by 7‐d exposure to the exhaust takes 4 wk, and recovery from elevated plasma formaldehyde and erythrocyte carboxyhemoglobin levels caused by a single 8‐h exposure takes 4–8 h.

ISSN:0098-4108    

DOI:10.1080/15287399309531755

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

The release of reactive oxygen intermediates (ROI) from bovine alveolar macrophages (BAM) after stimulation with heavy metal‐containing dusts was investigated. BAM were obtained by postmortem lavages of bovine lungs. The dusts were collected from waste incineration, sewage sludge incineration, an electric power station, and from two different factories. Three quartz dusts were used as heavy metal‐free controls. The dusts were fractionated by sieving and sedimentation and analyzed by electron microscopy, atomic absorption spectrometry (AAS), and atomic emission spectrometry with inductively coupled plasma (AES‐ICP). Incubation of BAM with the dusts (12.5–1000 μg/ml medium) led to concentration‐dependent increases in ROI release. The secretion of ROI was already seen after 15 min and lasted throughout the experiment up to 90 min, with the exception of a waste incinerator ash, which contained the highest contents of some heavy metals and where the release of ROI ceased after 60 min. We suggest that this dust exhibits simultaneously stimulating and inhibiting effects. The ratio of the secreted O−2and H2O2varied, depending on the dust being investigated. The release of hydrogen peroxide correlated best, in descending order, with the content of iron, manganese, chromium, vanadium, and arsenic in the dusts.

ISSN:0098-4108    

DOI:10.1080/15287399309531756

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

Naturally occurring glycoproteins have been extracted from fundic and antral mucosal tissue of the hog stomach by means of nondegrading techniques. Major and retarded glycoprotein fractions separated by gel filtration were further dissociated from appreciable amounts of noncovalently bound proteins by CsCl density gradient centrifugation. Antisera to glycoprotein fractions of fundic and antral regions of the stomach were prepared in rabbits. The major fractions from both gastric regions have similar molecular mass (∼2 × 106), sedimentation coefficient (∼31.5 s), and specific viscosity (∼1.6). Purified fractions from each region were further separated into two subfractions by affinity chromatography on wheat germ lectin. Clycoprotein subtractions from antrum and fundus differ appreciably in their carbohydrate and am/no acids content, share antigenic determinants, but do not cross‐react with anti‐hog serum protein anti‐sera. Further diversity in native mucin glycoproteins was observed by the use of one‐(D) and two‐dimensional (2D) immunoelectrophoresis; subtractions that cross‐react with specific anti‐hog gastric glycoproteins were found to contain three or more components.

ISSN:0098-4108    

DOI:10.1080/15287399309531757

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

Polychlorinated biphenyls (PCBs) are ubiquitous and persistent environmental pollutants. The major resident site for these PCBs is the soil, and human skin is frequently in contact with soil. Our objective was to determine the percutaneous absorption of the PCBs Aroclor 1242 and Aroclor 1254 from soil. PCB‐contaminated soil was prepared at levels of 44 ppm Aroclor 1242 and 23 ppm Aroclor 1254. PCB concentrations on skin were 1.75 μg/cm2for Aroclor 1242 and 0.91 μg/cm2for Aroclor 1254. In vivo percutaneous absorption in the rhesus monkey was determined by urinary and fecal [14CJ‐PCB excretion for a 5‐wk period following topical dosing. Absorption of Aroclor 1242 was determined in vitro with human skin for comparative purposes. In vivo in the rhesus monkey the percutaneous absorption of Aroclor 1242 was 13.8 ± 2.7 (SD)% of the dose and the absorption of Aroclor 1254 was 14.1 ± 1.0%. These absorption amounts are similar to the absorption of Aroclor 1242 and 1254 from other vehicles (mineral oil, trichlorobenzene, acetone). With in vitro percutaneous absorption through human skin, most of the Aroclor 1242 and Aroclor 1254 resided in the skin and the amounts were dependent upon dosing vehicle (water > mineral oil > soil). Both PCBs readily partitioned from water into soil and human powdered stratum corneum. By difference the partitioning favored both PCBs going from soil into stratum corneum. These data emphasize the role of soil in percutaneous absorption and provide information for appropriate risk assessment.

ISSN:0098-4108    

DOI:10.1080/15287399309531758

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

1,1,1‐Trichloro‐2‐propanone (1,1,1‐TCP) has been identified as a chlorination by‐product in finished drinking water supplies. Since little was known of its oral toxicity, exposure studies were conducted with male and female Sprague‐Dawley rats (10 males and 10 females/group) exposed by corn oil gavage at 0, 16, 48, 161, or 483 mg/kg for 10 d or 0, 30, 90, or 270 mg/kg for 90 d. Evaluations included mortality, clinical signs, body weight, food consumption, ophthalmology, hematology, clinical chemistry, urinalysis, organ weights, gross pathology, and histopathology.

ISSN:0098-4108    

DOI:10.1080/15287399309531759

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

摘要:

The effect of ad libitum dietary exposure (as occurs in the field) to parathion for 14 d was investigated on the muscarinic acetylcholine receptor (mAChR) in brains and submaxillary glands of adults of a field species, the white‐footed mouse Peromyscus leucopus. Immunoprecipitation using subtype selective antibodies revealed that the relative ratios of the m1‐m5 mAChR subtypes in Peromyscus brain were similar to those in rat brain. There was little variability in acetylcholinesterase (AChE) activity in control mice brains but large variability in 39 exposed mice, resulting from differences in food ingestion and parathion metabolism. Accordingly, data on radioligand binding to mAChRs in each mouse brain were correlated with brain AChE activity in the same mouse, and AChE inhibition served as a biomarker of exposure reflecting in situ paraoxon concentrations. Exposure to parathion for 14 d reduced maximal binding (Bmax) of [3H]quinuclidinyl benzilate ([3H]QNB), [3H]‐N‐methylscopolamine ([3H]NMS), and [3H]‐4‐diphenylacetoxy‐N‐methylpiperidine methiodide ([3H]‐4‐DAMP) by up to ∼58% without affecting receptor affinities for these ligands. Maximal reduction in Bmaxof [3H]QNB and [3H]‐4‐DAMP binding occurred in mice with highest AChE inhibition, while equivalent maximal reduction in Bmaxof [3H]NMS occurred in mice with only ∼10% AChE inhibition, without further change at higher parathion doses. This is believed to be due to the hydrophilicity of [3H]NMS, which limits its accessibility to internalized desensitized receptors. In submaxillary glands (mAChRs are predominantly m3 subtype), there were significant dose‐dependent reductions in [3H]QNB binding and m3 mRNA levels in exposed mice, revealed by Northern blot analyses. The reduction in m3 receptors is suggested to result mostly from reduced synthesis at the transcription level, rather than from translational or posttranslational events. The data suggest that down‐regulation of mAChRs occurs after dietary exposure (or 14 d to sublethal concentrations of parathion in a field rodent species, and that significant though incomplete recovery in AChE and mAChRs occurs in 7 d following termination of exposure.

ISSN:0098-4108    

DOI:10.1080/15287399309531760

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor

ISSN:0098-4108    

DOI:10.1080/15287399309531753

出版商:Taylor & Francis Group    

年代:1993

数据来源: Taylor