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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The work presents the results of investigations on the activity of beta-glucoronidase (B-GR) in neutrophiles and lymphocytes of peripheral blood in rats of Wistar strain exposed to benzene vapours of the concentration 27000 mg/m3, 6 hrs daily for 10 consecutive days. The activity of the enzyme in both types of cells was determined by cytochemical method; Hayashi et al. After an exposure to benzene, a statistically significant reduction of the number of granulocytes and lymphocytes was found. The activity of B-GR in granulocytes was lowered 5--times compared with the initial value (before exposure). The per cent of B-GR--positive lymphocytes was not changed. Instead, apparent changes in proportional values of individual types of enzyme--positive cells were found. The per cent of granular lymphocytes decreased, and at the same time the per cent of granular--diffusive and diffusive lymphocytes increased. The authors think that benzene affects granulocytes cells depressively and that it is an active labilisator of lysosomal lymphocytes. They set their hopes on the observed phenomenon to elaborate an exposure test to benzene.
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PMID:[Activity of beta-glucuronidase in peripheral blood leukocytes in rats subjected to subacute benzene vapor poisoning]. 59 37

In last decade it was suggested that the metabolism and toxicity of some xenobiotics may be modified by several compounds that alter the activities of microsomal oxidative and conjugating enzymes. In present study the effect of ethanol on benzene metabolism and benzene-induced hemotoxicity in pregnant rats was investigated. Pregnant female Wistar rats were exposed to benzene vapors for 6 hr/day from Days 8 through 15 of gestation at concentrations of 1500 and 3000 mg/m3 or combination ethanol and benzene at the same concentrations. Ethanol was administered intragastrically at a dose of 2.5 g/kg directly before exposure to benzene or 18 hrs before. An air-exposed or ethanol treated control rats were also studied. Before, during and after exposure blood samples for leukocyte and lymphocyte counts were obtained and urine for free phenol and conjugated phenol determinations was collected. Exposure to benzene alone decreased the maternal body weight and reduced leukocyte and lymphocyte counts in peripheral blood. Ethanol administered directly before exposure to benzene in principle had no effect on the metabolism and toxicity of benzene. It reduced the conversion of benzene to free and conjugated phenol, and protected animals from reduction of body weight and lymphopenia when was given 18 hrs before. Obtained results indicate that the early phases of benzene metabolism and its toxicity may be modified by ethanol.
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PMID:[Modification of metabolism and toxicity of benzene by ethanol in pregnant rats]. 184 23

Toxicity of environmental pollutants may be expressed as combined effects of a chemicals. Benzene, a proven hematotoxic agent, frequently occurs with toluene in cocontaminated groundwater. Groups of CD-1 male mice were exposed continuously for 4 weeks to benzene (166 mg/l), toluene (80 and 325 mg/l), and combinations of benzene (166 mg/l) + toluene (80 mg/l or 325 mg/l) in drinking water. Benzene-induced anemia was alleviated by simultaneous toluene treatment. Leukopenia and lymphopenia were observed in the case of benzene only and benzene + toluene (80 mg/l)-treated mice. The cytopenia, however, was less severe in the benzene + toluene (325 mg/l)-treated group. Immunotoxicity induced by benzene treatment alone was characterized by involution of thymic mass and suppressions of both B- and T-cell mitogeneses, mixed lymphocyte culture response to alloantigens, the tumor lytic ability of cytotoxic T-lymphocytes as determined by 51Cr-release assay, and antibody production response to T-dependent antigen (sheep red blood cells). IL-2 secretion by Con A-stimulated mouse T-cells was decreased in the benzene-treated group. Toluene (325 mg/l) completely inhibited these adverse effects when it was coadministered with benzene, while the low dose of toluene (80 mg/l) did not protect against benzene-induced depressions of immune functions. Toluene administered alone at levels up to 325 mg/l showed no obvious immunotoxic effects. Results of this study demonstrated that toluene, in sufficient amounts, has an antagonistic effect on benzene immunotoxicity.
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PMID:Subclinical effects of groundwater contaminants. III. Effects of repeated oral exposure to combinations of benzene and toluene on immunologic responses in mice. 214 47

CBA/Ca male mice were given 3'-azido-3'-deoxythymidine (AZT) in drinking water (1 mg/ml) for up to 7 weeks. Water consumption and body weight decreased significantly. Neutropenia and lymphopenia were observed during and after exposure. Significant macrocytic anemia developed and disappeared as a function of red cell life span after stopping AZT intake. A microthrombocytosis was seen. Bone marrow cellularity and spleen colony-forming unit (CFU-s) content fell, but recovered completely and quickly after terminating AZT intake. Hemopoietic stem cell function measured by 2 different methods of rescuing fatally irradiated mice was normal 4 weeks after AZT exposure, suggesting that AZT treatment does not induce a long-lasting effect in genetic control of mitotic potential of stem cells. This is in marked contrast to exposure of CBA/Ca mice to benzene and ionizing radiation.
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PMID:In vivo toxicity of 3'-azido-3'-deoxythymidine (AZT) on CBA/Ca mice. 223 Feb 84

CBA/Ca male mice have been exposed to benzene in air at 10, 25, 100, 300, 400, and 3000 ppm for variable intervals 6 hr/day, 5 days/week for up to 16 weeks. Two weeks of inhaling 10 ppm produced no hematologic effects; 25 ppm induced a significant lymphopenia. Inhalation of 100, 300, and 400 ppm produced dose-dependent decreases in blood lymphocytes, bone marrow cellularity, marrow content of spleen colony-forming units (CFU-S) and an increased fraction of CFU-S in DNA synthesis. Exposure of mice to 300 ppm for 2, 4, 8, and 16 weeks produced severe lymphopenia and decrease in marrow CFU-S. Recovery was rapid and complete after 2 and 4 weeks of exposure. After 8 and 16 weeks of exposure, recovery of lymphocytes was complete within 8 weeks. It took 16 weeks for the CFU-S to recover to that of the age-matched controls after 8 weeks of exposure and 25 weeks to recover to age-matched after 16 weeks of exposure. Inhalation of 3000 ppm for 8 days was less damaging than inhalation of 300 ppm for 80 days (same integral amount of benzene inhaled). The inhalation of 3000 ppm has not increased the incidence of leukemia or shortened its latency for development. Inhalation of 300 ppm 6 hr/day for 16 weeks significantly increases the incidence of myelogenous neoplasms in male CBA/Ca mice. Inhalation of 100 ppm for same interval does not influence incidence of myelogenous neoplasms but does increase incidence of solid neoplasms particularly in female CBA/Ca mice. Benzene is a potent carcinogen in CBA/Ca mice.
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PMID:Hematotoxicity and carcinogenicity of inhaled benzene. 279 54

Female BDF1 mice were exposed for 16 weeks to airborne concentrations of 100, 300, and 900 ppm of benzene, 6 h per day, 5 days per week. Bone marrow hemopoietic stem cell compartments and peripheral blood cell counts were studied using clonal assays and standard methods. Dose-dependent depressive effects were observed on all stem cell compartments. Only the erythroid colony-forming units (CFU-E) compartment was depressed during exposures to 100 ppm; CFU-E were more sensitive than the erythroid burst-forming units (BFU-E), spleen CFU (CFU-S), or G-M CFU (CFU-C) during exposure to 300 ppm or 900 ppm. Lymphocytopenia was observed in the peripheral blood. After benzene-free intervals, a regeneration of lymphocyte numbers and slow normalization of stem cell numbers was seen. Complete recovery from the 16 weeks exposure to 300 ppm was seen between 73 and 185 days.
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PMID:The hematopoietic stem cell compartments in mice during and after long-term inhalation of three doses of benzene. 291 24

Benzene is ubiquitous and accepted as a human carcinogen by regulatory agencies. Proposed regulations assume without proof that the carcinogenic response to benzene exposure is "one hit" implying a linear with no threshold. There is no solid experimental proof for this concept. This research involves exposure of CBA/Ca male mice to benzene vapor in varying concentrations. Exposure to 300 ppm 6 hrs/day, 5 days/week, for 16 weeks is highly leukemogenic. Exposure for the same time to 100 ppm is also leukemogenic. Concentrations from 25 ppm to 400 ppm 6 hrs/day, 5 days/week, for 10 exposures produce an increasing lymphopenia. Exposure to 100 ppm for the same exposure time produces anemia, decrease in stem cell content of marrow, and marrow cellularity. Further dose-effect studies are required to test the "one hit hypothesis" and to determine whether the same integral dose of benzene administered over variable exposure has the same or different biological responses. It is of concern that biologic effects are observed at 25 ppm only 2.5 times the present permissible time-weighted average exposure during a working day and research by others (see Discussion) has demonstrated an effect (noncarcinogenic) at 10 ppm.
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PMID:Benzene hematotoxicity and leukemogenesis. 379 Jul 32

The toxic effects of environmental factors at work places on the hematopoietic and immune systems are of basic importance due to the time of exposure, lasting on average 8 hours daily during one week. Porphyrinurias and porphyrias have been observed after exposure to hexachlorobenzene, chlorinated dibenzodioxins, polychlorinated biphenyls, polybrominated biphenyls, vinyl chloride and lead. Aplastic anemia may occur after exposure to benzene, pesticides, arsenic, cadmium and copper compounds. Megaloblastic anemia has been noted in subjects exposed to arsenic, chlordane, benzene and nitrous oxide. Methemoglobinemia is induced by aromatic nitro and amino compounds. Hemolytic reactions caused by arsenic, methyl chloride, naphthalene, lead, cadmium and mercury compounds represent a separate problem. Immunodeficiencies resulting in decreased antitumor and antiinfectious immunity have been reported in subjects exposed to asbestos, ozone, dimethylsulphoxide, vinilidene chloride, and benzene homologues. Lymphocytopenia may be induced by manganese, lead, toluene and industrial noise. Neutropenia was marked after exposure to carbon disulphide, arsenic compounds, benzene and electromagnetic fields. Only a few reports concern the lymphocyte T3, T4 and T8 subpopulations. Electromagnetic fields (microwaves) cause an imbalance of that subpopulation, consisting of a decrease in the T8 cell count. The neutrophil enzymes, such as myeloperoxidase and alkaline phosphatase, decrease in their activity after exposure to polychlorinated biphenyls, carbon disulphide, chlorobenzene and DDT. A majority of agents cited include genotoxic effects reflected in chromosome aberrations and increased sister chromatid exchange and abnormal unscheduled DNA synthesis. Leukemia or lymphoma risk is increased after exposure to pesticides, electromagnetic fields, benzene and irradiation.
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PMID:Immunotoxic and hematotoxic effects of occupational exposures. 817 62

A study was carried out into the hematological abnormalities of peripheral blood bone marrow in patients chronically exposed to benzene. The metabolic biotransformation and the mechanisms involved in toxicity are described. Hematological data are described and discussed. Macrocytosis and lymphopenia are the earliest hematological signs of benzene toxicity. Bone marrow abnormalities are demonstrated by the complementary methods of cytology and histology. Global hypocellularity was mainly due to the granulocytic series. Mastocytosis, eosinophilia and magakariocytic abnormalities are also presented. Inflammatory abnormalities and signs of dismyelopoiese could also be observed. The importance of peripheral blood abnormalities and the need for a critical approach to this important public health problem are emphasized.
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PMID:[Hematologic changes in patients chronically exposed to benzene]. 827 83

Whether low-level benzene exposure produces health effects is controversial. We used routinely collected data from our medical/industrial hygiene system to study 387 workers with daily 8-hour time-weighted exposures averaging 0.55 ppm. The cross-sectional repeated survey design included 553 unexposed workers. Lymphopenia is considered to be the earliest and most sensitive indicator of benzene toxicity. We found no increase in the prevalence of lymphopenia among benzene-exposed workers (odds ratio, 0.6; 95% confidence interval, 0.2 to 1.8), taking into account smoking, age, and sex. There also was no increase in risk among workers exposed 5 or more years (odds ratio, 0.6; 95% confidence interval, 0.2 to 1.9). Examination of other measures of hematotoxicity, including mean corpuscular volume and counts of total white blood cells, red blood cells, hemoglobin, and platelets, produced similar results. We conclude that risk of lymphopenia and other early indicators of hematotoxicity are not increased among workers in this study who were exposed to low levels of benzene.
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PMID:Evaluation of lymphopenia among workers with low-level benzene exposure and the utility of routine data collection. 909 75


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