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1. |
Lead in human blood and milk from nursing women living near a smelter in Mexico City |
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Journal of Toxicology and Environmental Health,
Volume 38,
Issue 3,
1993,
Page 225-232
D. Namihira,
L. Saldivar,
N. Pustilnik,
G. J. Carreón,
M. E. Salinas,
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摘要:
Lead levels in breast milk and blood were determined in women living within a 200‐m radius of 3 smelters in Mexico City. All samples were analyzed on a Perkin Elmer 460 atomic absorption spectrometer equipped with HCA 2200. The mean blood lead level was 45.88 μg/dl (SD 19.88 ng/dl), and the geometric mean of milk lead level was 2.47 μg/100 ml. The correlation coefficient of these two variables was 0.88. Using the mean value of lead found in breast milk, an infant of 5.5 kg would ingest 8.1 μg/kg/d in his diet. The daily permissible intake (DPI) established by the World Health Organization (WHO) in 1972 for an adult is 5.0 μg/kg/d.
ISSN:0098-4108
DOI:10.1080/15287399309531714
出版商:Taylor & Francis Group
年代:1993
数据来源: Taylor
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2. |
Urinary excretion of unmetabolized benzene as an indicator of benzene exposure |
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Journal of Toxicology and Environmental Health,
Volume 38,
Issue 3,
1993,
Page 233-243
S. Ghittori,
M.L. Fiorentino,
L. Maestri,
G. Cordioli,
M. Imbriani,
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摘要:
Benzene concentrations in urine samples (Cu, ng/L) from 110 workers exposed to benzene in chemical plants and gasoline pumps were determined by injecting urine supernate into a gas chromatograph. The urine was saturated with anhydrous N2SO4to facilitate the passage of benzene in the air over the urine. The solvent was stripped from the urine surface and concentrated on an adsorbent substrate (Carbotrap tube) by means of a suction pump (flow rate 150 ml/m). Wash‐up of the head space was achieved by simultaneous intake of filtered air through charcoal. Benzene was thermi‐cally desorbed and injected in a column (thermal tube desorber, Supelco; 370°C thermal flash; borosilicate capillary glass column SPB‐1, 60 m length, 0.75 mm ID, 1 pm film thickness; GC Dani 8580‐FID). Benzene concentrations in the urine from 40 non‐exposed subjects (20 smokers > 20 cigarettes/d and 20 nonsmokers) were also determined [median value of 790 ng/L (10.17 nmol/L) and 131 ng/L (1.70 nmol/L), respectively]. The 8‐h time‐weighted exposure intensity (Cl, ng/m3) of individual workers was monitored by means of charcoal tubes. The median value for exposure to benzene was 736 ng/m3(9.42 μmol/m3) [geometric standard deviation (CSD) ‐ 2.99; range 64 μg/m3(0.82 μmol/m3) to 13,387 μg/m3) (171.30 μmol/m3)]. The following linear correlation was found between benzene concentrations in urine (Cu, ng/L) and benzene concentrations in the breathing zone (Cl, μg/m3):
ISSN:0098-4108
DOI:10.1080/15287399309531715
出版商:Taylor & Francis Group
年代:1993
数据来源: Taylor
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3. |
Distribution of glass fibers in the peritoneal cavity of the rat following administration by intraperitoneal injection |
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Journal of Toxicology and Environmental Health,
Volume 38,
Issue 3,
1993,
Page 245-256
A. Morgan,
C. G. Collier,
J. P. Kellington,
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摘要:
The distribution of glass fibers in the peritoneal cavity of the rat was investigated at 2, 24, and 48 h following intraperitoneal injection of 7 mg of material using a radioactive tracer technique. At each time point the peritoneal cavities of the rats killed were lavaged with 20 ml of physiological saline to recover fibers not yet attached to tissue surfaces. At 2 h, 35% of the administered fiber could be recovered by lavage, but at 48 h this was reduced to 2%. At 48 h, the amount of fiber associated with the abdominal organs and the abdominal wall was roughly in proportion to their surface areas. The weight of fiber associated with the various tissues was in the following order: gastrointestinal tract > liver > carcass (abdominal wall) > diaphragm > urogenital tract > spleen > kidneys.
ISSN:0098-4108
DOI:10.1080/15287399309531716
出版商:Taylor & Francis Group
年代:1993
数据来源: Taylor
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4. |
Strain comparisons of DFP neurotoxicity in rats |
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Journal of Toxicology and Environmental Health,
Volume 38,
Issue 3,
1993,
Page 257-271
ChristopherJ. Gordon,
RobertC. MacPhail,
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摘要:
The purpose of this study was to assess intraspecies differences in behavioral and autonomic function in three strains of rat following administration of diisopropyl fluorophosphate (DFP), an irreversible inhibitor of acetylcholinesterase activity. Male rats of the Long‐Evans (LE), Fischer 344 (F344), and Sprague‐Dawley (SD) strains were administered DFP at doses of 0–1.5 mg/kg (sc). The animals were placed 60 min later into one of two motor activity chambers and tested for 30 min. Motor activity was measured using either a Doppler‐based system or a commercial photocell device. Following measurement of motor activity in the Doppler system, body temperature (Tb) was measured and blood was then withdrawn by cardiac puncture and analyzed for serum cholinesterase activity (ChE). The remaining rats were retested 1 d after DFP administration in the photocell device. The results showed a significant influence of strain on the effects of DFP. Motor activity of LE rats was reduced by DFP at doses of 1.0 and 1.5 mg/kg, whereas the activity of F344 rats was reduced only at 1.5 mg/kg. The relative sensitivity of SD rats depended on the device used to measure motor activity. The SD rats resembled F344 rats in their response to DFP when motor activity was measured in the photocell device, and LE rats when motor activity was measured in the Doppler system. The Tbof F344 rats was unaffected by DFP, while the LE and SD rats became hypothermic at 1.5 mg/kg. The DFP‐induced inhibition of serum ChE activity was significantly less in F344 rats. All three strains retested the day after DFP still showed significant decreases in motor activity. Overall, it appears that the F344 strain is relatively resistant to the behavioral and autonomic effects of DFP. This intraspecies variability should be considered in selecting appropriate experimental models for assessing the neurotoxicological hazards of cholinesterase‐inhibiting pesticides.
ISSN:0098-4108
DOI:10.1080/15287399309531717
出版商:Taylor & Francis Group
年代:1993
数据来源: Taylor
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5. |
Depression of stimulated arachidonate metabolism and superoxide production in rat alveolar macrophages following in vivo exposure to 0.5 PPM NO2 |
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Journal of Toxicology and Environmental Health,
Volume 38,
Issue 3,
1993,
Page 273-292
TimothyW. Robison,
JudithK. Murphy,
LindaL. Beyer,
Arnis Richters,
HenryJay Forman,
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摘要:
Alveolar macrophages (AM) have been found to suffer significant functional deficits in response to nitrogen dioxide (NO2) exposure. The present investigation examined changes in the activation of AM arachidonate metabolism and superoxide production in response to an environmentally relevant level of NO2. Rats were exposed to 0.5 ppm NO2for periods of 0.5–10 d and AM were obtained by bronchoalveolar lavage (BAL). NO2exposure produced complex effects upon both unstimulated and stimulated AM arachidonate metabolism. Unstimulated AM synthesis of leukotriene B4(ITB4) was depressed rapidly within 1 d of exposure, and depressed again at 5 d. Alveolar macrophage production of thromboxane B2(TxB2), LTB4, and 5‐hydroxyeicosatetraenoate (5‐HETE) in response to stimulation with the calcium ionophore, A23187, were acutely depressed within 1 d of exposure; however, generation of these compounds recovered to air‐control levels with longer exposure, while 5‐HETE was increased at 10 d. In contrast, AM production of LTB4in response to another stimulus, zymosan‐activated rat serum (ZAS), was not depressed until following 5 d of exposure and remained slightly lower than air‐control levels at 10 d. Levels of TXB2, LTB4prostaglandin E2(PGE2), and prostaglandin F2α(PCF2α) measured in BAL fluid (BALF) were found to be depressed within 4 h of exposure, suggesting an acute decrease in the in vivo pulmonary arachidonate metabolism; however, production of these compounds generally recovered to air‐control levels with longer exposure. The AM superoxide production stimulated by phorbol myristate acetate (PMA) was decreased rapidly and continuously throughout the study. Thus, exposure to a low concentration of NO2acutely depresses activation of AM arachidonate metabolism and superoxide production in response to external stimuli, and may impede defense against pulmonary infection.
ISSN:0098-4108
DOI:10.1080/15287399309531718
出版商:Taylor & Francis Group
年代:1993
数据来源: Taylor
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6. |
Hepatocyte cell proliferation in mice after inhalation exposure to unleaded gasoline vapor |
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Journal of Toxicology and Environmental Health,
Volume 38,
Issue 3,
1993,
Page 293-307
Lorraine Tilbury,
ByronE. Butterworth,
Owen Moss,
ThomasL. Goldsworthy,
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摘要:
Chronic inhalation exposure to unleaded gasoline (UC) induced an increase in liver tumors in female but not male mice. Unleaded gasoline exhibits little, if any, genotoxic activity in vitro or in vivo in the female mouse liver, suggesting that other biological effects such as the induction of cell turnover or altered growth control may play a role in this carcinogenic process. To better understand the role of UG‐induced hepatocyte proliferation with respect to the dose‐ and sex‐specific tumor response, male and female B6C3F1 mice were housed in 1‐m3single‐pass flow‐through inhalation chambers and administered UC under exposure conditions that produced tumors in the chronic studies. Mice were exposed to targeted concentrations of 67, 292, or 2056 ppm PS‐6 blend of UC vapor 6 hid, 5 d/wk, for up to 13 wk. Liver weights were elevated significantly in male and female mice exposed to 2056 ppm UC at wk 1, 3, 6, and 13. No elevation in liver‐specific serum enzymes was noted in treated animals, nor were there any significant histopathological changes in the liver, indicating a lack of overt hepatotoxicity. Hepatocyte proliferation, expressed as nuclear labeling index (LI), was measured immunohistochemically after 5‐bromo‐2'‐deoxyuridine administration via an osmotic minipump implanted three days before the animals were killed. A 6‐to 10‐fold increase in LI compared to controls was observed in male and female mice exposed to 2056 ppm UC at wk 1, with a return to control levels at wk 3, 6, and 13. Mice exposed to 67 or 292 ppm UC did not show any increase in LI. The mode by which an agent induces cell proliferation is an important consideration in mechanistic studies and the risk assessment process. These data indicate an early transient mitogenic stimulation of cell proliferation, rather than regeneration secondary to cytotoxicity, in the livers of UG‐treated mice. The observed proliferative response after UC exposure in the male mouse in the absence of a tumorigenic response suggests that effects in addition to the early transient hepatocyte proliferation response are critical in understanding the sex‐specific hepatocarcinogenic response of this complex mixture.
ISSN:0098-4108
DOI:10.1080/15287399309531719
出版商:Taylor & Francis Group
年代:1993
数据来源: Taylor
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7. |
Fumonisins‐mycotoxins produced byfusarium moniliforme |
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Journal of Toxicology and Environmental Health,
Volume 38,
Issue 3,
1993,
Page 309-328
WilliamP. Norred,
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摘要:
Fumonisins are toxic metabolites of the fungus Fusarium moniliforme, which is a common contaminant of corn everywhere in the world. The fumonisins are carcinogenic in laboratory rats, and cause acute toxicity of domestic animals that mimics field cases of disease attributed to contamination of feed by F. moniliforme. These include both equine leukoencephalomalacia and porcine pulmonary edema. Fusarium moniliforme contamination of corn consumed by humans in certain areas of the world is associated with higher than average incidence of esophageal cancer, and fumonisins may be responsible. Analytical methods have been developed for fumonisins, but improvements are needed so that more accurate, less expensive, and more rapid assays of food and feedstuffs can be done. Fumonisins are structurally similar to sphingosine, and may exert their biological activity through their ability to block key enzymes (sphinganine‐ and sphingosine‐N‐acyltransferases) involved in sphingolipid biosynthesis. Much more research is needed to define the extent to which this myco‐toxin adversely affects the food supply, and its involvement in animal and human diseases.
ISSN:0098-4108
DOI:10.1080/15287399309531720
出版商:Taylor & Francis Group
年代:1993
数据来源: Taylor
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8. |
Astrocytes: Targets and mediators of chemical‐induced cns injury |
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Journal of Toxicology and Environmental Health,
Volume 38,
Issue 3,
1993,
Page 329-342
Michael Aschner,
RichardM. LoPachin,
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摘要:
It is now well established that a reciprocal relationship exists between neurons and astrocytes, and that this association is vital for mutual differentiation, development, and functioning of both cell types. It had also become apparent that perturbations in astrocytic function may lead to deleterious consequences in juxtaposed neurons. It is therefore possible that neuronal damage induced by chemicals or neuropathic disease involves dissociation of astrocytic‐neuronal interactions. The purpose of this review is to explore astrocytic‐neuronal interactions, focusing on potential sites of neurotoxicant actions. In developing this thesis, we briefly examine the functional interactions between astrocytes and neurons, followed by specific examples of astrocyte‐mediated neurotoxicity.
ISSN:0098-4108
DOI:10.1080/15287399309531721
出版商:Taylor & Francis Group
年代:1993
数据来源: Taylor
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9. |
Editorial board |
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Journal of Toxicology and Environmental Health,
Volume 38,
Issue 3,
1993,
Page -
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ISSN:0098-4108
DOI:10.1080/15287399309531713
出版商:Taylor & Francis Group
年代:1993
数据来源: Taylor
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