[The effect of inhalation exposure to phenolformaldehyde and melamine bitumens on HDL cholesterol levels in humans (author's transl)].
Explore the source record for details and available documents.
Adhesives↗
SEARCH · Search PubMed
Results for “Inhalation Exposure”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Neurobehavioral effects of methyl bromide inhalation exposures.
Methyl bromide, a neurotoxic agent with a permissible US exposure limit of 20 ppm, is used primarily as a fumigant by an estimated 75,000 workers in the United States. This project was developed to evaluate the neurobehavioral effects of chronic and subchronic exposure to methyl bromide. One group of rats and rabbits was exposed to 65 ppm of methyl bromide for a total exposure of four 25-h weeks, or 100 h, and rats were exposed to 55 ppm of methyl bromide for a total exposure of 36 30-h weeks, or 1,080 h. Comparable control groups were given similar treatment, but no exposure. Behavioral tests of open field activity and limb coordination were conducted weekly during both phases of the experiment with rats, and eyeblink reflexes were measured weekly in rabbits. Nerve conduction velocity measurements were taken weekly from both rats and rabbits during the 65-ppm four-week exposures and monthly from rats during the 55-ppm 40-week exposures. Exposure to 65 ppm for four weeks significantly reduced eyeblink responses and nerve conduction velocity in rabbits but had no effect on rats. Exposure to 55 ppm of methyl bromide for 36 weeks had no effect on nerve conduction velocity, open-field activity, or coordination in rats.
Animals↗
Accumulation of styrene monomer and neurochemical effects of long-term inhalation exposure in rats.
A simplified compartment model indicated that fat styrene content might be used as an index of the whole body styrene burden. Intermittent exposure of adult male rats to 300 ppm 5 d a week, 6 h daily for 1 to 11 weeks showed an initial steady increase in the fat styrene content up to the 4th week and an exponential decrease thereafter. This phenomenon might have resulted from the enhancement of styrene oxidation due to the prolonged exposure. The effect of the increased oxidation on the body styrene burden is theoretically doubled after 9.1 weeks of exposure. Neurochemical effects after that time might have resulted from an increased binding of styrene oxide in the cellular macromolecules, e.g., to their sulfhydryl groups. The activity of the metabolite towards the cellular constituents could very well explain the increased proteolysis possibly caused by lysosomal labilization. The present data also lend support to the theory of the importance of metabolic activation to styrene and other solvent toxicity.
Adipose Tissue↗
Assuring quality in inhalation exposure research.
Explore the source record for details and available documents.
Air Pollutants↗
Interaction of styrene and ethylmethylketone in the induction of cytochrome P450 enzymes in rat lung, kidney and liver after separate and combined inhalation exposures.
The present study compares the induction of different cytochrome P450 forms (CYP1A1/2, 2B1, 2E1) after pretreatment with styrene, ethylmethylketone separately or in combined exposures. Combined exposures lead to cumulative elevation of CYP levels, except for CYP1A1 and 2B1. Induction of CYP1A1 was higher in liver and kidney respectively and did not change significantly with the pretreatment mode. Styrene produced two times higher induction of CYP1A2 in the lung and kidney than ethylmethylketone. The simultaneous application of both inducers lead to significantly higher induction of CYP1A2 than that estimated after pretreatment with each of the inducers separately. CYP2B1 was induced by styrene to higher extent in the liver, where it was almost indetectable in controls. Major form of cytochrome P450 induced by styrene proved to be CYP2E1--about 3-fold induction of chlorzoxazone hydroxylation activity in the liver and 2.5 times in the lung. Ethylmethylketone significantly potentiated the CYP2E1 induction ability of styrene. This induction of CYP2E1-dependent catalytic activity correlates with the enzyme levels detected by immunoblotting.
Animals↗
[A qualitative evaluation of health risk associated with occupational inhalation exposure to cadmium in production plants in Poland].
In Poland several thousand people work under exposure to cadmium with different concentrations. The concentrations observed range between the level which is not determinable and the level above 0.3 mg/m3, at the MAC value equal to 0.04 mg/m3. In 1993 the cadmium classification was modified by the International Agency for Research on Cancer (IARC). Previously cadmium had been proved to be carcinogenic to animals (group 2B). At present it is classified in group 1, namely in the group of substances proved to be carcinogenic to humans. The cadmium MAC value, mandatory in Poland, has been set on the basis of the data on its chronic, toxic renal effects, but its critical effect in the form of cancer has not been taken into consideration. The author, using the results of epidemiological studies carried out by Thun et al., presented three dose-response functions which describe the relationship between the size of exposure and the probable incidence of lung cancer. The author used a linear multistage model, a Poisson model and a Cox proportional-hazards model; the magnitude of the risk from occupational exposure to concentrations equal to MAC values (0.04 mg/m3) was different for each model and it accounted for 9.02 x 10(-3), 2.04 x 10(-2) and 4.68 x 10(-2), respectively. Each of these values exceeded the acceptable level of the risk from occupational exposure which usually falls within 10(-3).
Cadmium↗
[Quantitative evaluation of health risk associated with occupational inhalation exposure to vinyl chloride at production plants in Poland].
Vinyl chloride is classified by the IARC in group 1-human carcinogens. In Poland occupational exposure to vinyl chloride is found among workers employed in many branches of industry, among others in the industry of vinyl chloride synthesis and polymerization as well as in the plastics, footwear, rubber, pharmaceutical and metallurgical industries. Concentrations observed range from the noon-determinable level to 90 mg/m3, at the MAC value equal to 5 mg/m3. Neoplasm of liver is a major carcinogenic effect of vinyl chloride. Hence, the health assessment focused on this critical risk. Four different linear dose-response models, developed by several authors and based on results of different epidemiological studies, were used to characterise the extent of cancer risk depending on the level of vinyl chloride concentrations. The estimated risk related to a forty-year employment under exposure equal to MAC values (5 mg/m3) fell within the range from 2.9.10(-4) to 2.6.10(-3). As the figures depict it did not exceed the acceptable level (10(-3)).
Air Pollutants, Occupational↗
239PuO2 aerosol inhalation exposure of miniature swine.
Explore the source record for details and available documents.
Aerosols↗
Tissue manganese concentrations in lactating rats and their offspring following combined in utero and lactation exposure to inhaled manganese sulfate.
There is little information regarding the tissue distribution of manganese in neonates following inhalation. This study determined tissue manganese concentrations in lactating CD rats and their offspring following manganese sulfate (MnSO4) aerosol inhalation. Except for the period of parturition, dams and their offspring were exposed to air or MnSO4 (0.05, 0.5, or 1 mg Mn/m3) for 6 h/day, 7 days/week starting 28 days prior to breeding through postnatal day (PND) 18. Despite increased manganese concentrations in several maternal tissues, MnSO4 inhalation exposure did not affect body weight gain, terminal (PND 18) body weight, or organ weights in the dams. Exposure to MnSO4 at 1 mg Mn/m3 resulted in decreased pup body weights on PND 19 and decreased brain weights in some PND 14 to PND 45 pups. Exposure to MnSO4 at > or =0.05 mg Mn/m3 was associated with increased stomach content, blood, liver, and skull cap manganese concentrations in PND 1 pups, increased brain, lung, and femur manganese concentrations in PND 14 pups, and elevated olfactory bulb, cerebellum, and striatum manganese concentrations in PND 19 pups. When compared to controls, MnSO4 exposure to > or =0.5 mg Mn/m3 increased liver and blood manganese concentrations in PND 14 pups and increased liver, pancreas, and femur manganese concentrations in PND 19 pups. Manganese concentrations returned to control values in all offspring tissues by PND 45 +/- 1. Our data demonstrate that neonatal tissue manganese concentrations observed following MnSO4 inhalation are dependent on the MnSO4 exposure concentration and the age of the animal.
Administration, Inhalation↗
Inhalation efficacy of RFI-641 in an African green monkey model of RSV infection.
Human respiratory syncytial virus (RSV) is a major cause of acute upper and lower respiratory tract infections. RFI-641 is a novel RSV fusion inhibitor with potent in vitro activity. In vivo efficacy of RFI was determined in an African green monkey model of RSV infection involving prophylactic and therapeutic administration by inhalation exposure. Inhalation was with an RFI-641 nebulizer reservoir concentration of 15 mg/ml for 15 minutes (short exposure) or 2 hours (long exposure). Efficacy and RFI-641 exposure was determined by collection of throat swabs, nasal washes and bronchial alveolar lavage (BAL) on selected days. The short-exposure group (15 minutes) exhibited no effect on the nasal, throat or BAL samples. The throat and nasal samples for the long-exposure group failed to show a consistent reduction in viral titers. RFI-641 2 hours exposure-treated monkeys showed a statistically significantly log reduction for BAL samples of 0.73-1.34 PFU/ml (P-value 0.003) over all the sampling days. Analysis indicates that the long-exposure group titer was lower than the control titer on day 7 and when averaged across days. The results of this study demonstrate the ability of RFI-641 to reduce the viral load of RSV after inhalation exposure in the primate model of respiratory infection.
Administration, Inhalation↗
Exposure levels and determinants of inhalable dust exposure in bakeries.
The study's objectives were to measure full-shift exposure to inhalable dust in bakeries and define the determinants of full-shift exposure. Inhalable dust was measured gravimetrically. Ninety-six bakery workers, employed in seven different bakeries, participated in the study. Two side-by-side full-shift inhalable dust samples were obtained from each study participant on a single occasion. Samples were collected on 18 days selected at random. During the entire sampling period, bakers were observed and information on 14 different tasks was recorded at 15 min intervals. Other production characteristics were also recorded for each sampling day. These task and production variables were used in statistical modelling to identify significant predictors of exposure. The mean full-shift inhalable dust exposure was 8.2 mg/m3 (range: 0.1-110 mg/m3). A regression model explained 79% of the variability in exposure. The model indicated that tasks such as weighing, pouring and operating dough-brakers and reversible sheeters increased the exposure, while packing, catching and decorating decreased the exposure. Bread and bun production lines were associated with increased full-shift inhalable dust exposure, while cake production and substitution of dusting with the use of divider oil were associated with decreased exposure. Production tasks and characteristics are strong predictors of personal full-shift exposures to flour dust among bakers; these can be altered to reduce exposure levels.
Analysis of Variance↗
Pulmonary irritant potency of polyisocyanate aerosols in rats: comparative assessment of irritant threshold concentrations by bronchoalveolar lavage.
The object of this study was to compare the relative acute pulmonary irritant potency of respirable aerosols of a variety of non-volatile polyisocyanates. The types of polyisocyanates examined included aliphatic homopolymers and mixed aliphatic-aromatic polyisocyanates consisting of the following monomers: HDI (hexamethylene 1,6-diisocyanate), IPDI (isophorone diisocyanate), MDI (methylene-diphenyl-4,4'-diisocyanate) and TDI (toluene diisocyanate). For reference purposes, the pulmonary irritant polyisocyanate aerosols were compared with monomeric IPDI, a semi-volatile respiratory tract (airway) irritant. In the substances tested, the concentration of free isocyanate moieties ranged from 11% to 38%. The relative potency to elicit pulmonary irritation was assessed by measurements of lung weights and total protein and lactate dehydrogenase (LDH) in the bronchoalveolar lavage fluid (BALF) following a single 6-h exposure of male rats. The time course of changes was analysed 3 h and 1, 3 and 7 days after exposure. When exposed to irritant concentrations of aerosol, BALF protein was maximal on post-exposure day 1 and returned to the level of the controls on post-exposure day 7. In contrast, rats exposed to sub-lethal concentrations of monomeric IPDI experienced a time-related increase in BALF protein. Based on this most sensitive endpoint, extrapolated no-observed-effect concentrations (NOECs) were in the range of 2-3 mg m(-3) for most polyisocyanates examined. The NOECs from all the substances investigated were in the range 1-50 mg m(-3). Thus, this methodology is adequate to rank the pulmonary irritant potency of polyisocyanate aerosols and to differentiate pulmonary from airway irritants. For pulmonary irritants the estimated acute NOECs were essentially similar to the no-observed-adverse effect concentrations (NOAECs) from long-term, repeated-exposure inhalation studies available for some of the polyisocyanates. A clear dependence of the NOAECs on the content of free isocyanate moieties was not observed. In summary, it is concluded that pulmonary irritation caused by polyisocyanate aerosols can be quantified readily in an acute rat bioassay by analysis of total protein in BALF. Moreover, this experimental evidence suggests that the NOECs of pulmonary irritants based on this endpoint are predictive of the NOAECs observed after subacute/subchronic inhalation exposure, suggesting that acute pulmonary irritation governs the outcome of repeated inhalation studies with such aerosols. However, for isocyanates where airway irritation predominates the pulmonary irritation, long(er)-term inhalation studies appear to be indispensable. The content of free NCO per se appears to be a poor predictor of the pulmonary irritant potency of polyisocyanate aerosols.
Administration, Inhalation↗
Particle toxicology: from coal mining to nanotechnology.
Particle research has been historically closely connected to industrial activities or materials, such as coal, asbestos, man-made mineral fibers, and more recently ambient particulate matter (PM). It is the purpose of this review to combine insights and developments in particle toxicology with the historical context of exposure and organizations sponsoring such research in Europe. In supporting research on particle-induced respiratory effects and mechanisms, research programs of the European Community on Steel and Coal (ECSC) have played a tremendous role. Current particle research in Europe is dominated by PM, and funded by the World Health Organization (WHO), European Union Framework programs, and the Health Effects Institute (HEI). Differences between historical and current research in particle toxicology include the exposure concentrations, particle size, target populations, endpoints, and length of exposure. Inhaled particle effects are no longer confined to the lung, since particles are suggested to translocate to the blood while lung inflammation invokes systemic responses. Finally, the particle size and concentrations have both been reduced about 100-fold from 2-5 mg/m3 to 20-50 mg/m3 and from 1-2 microm to 20-100 nm (ultrafine) as domestic fuel burning has decreased and vehicle sources have increased and attention has moved from coal mining industry to general environment. There is, however, a further occupational link to nanotechnology, which continuously produces new materials in the ultrafine range. Although inhalation exposure is considered to be minimal in this technology, some particles are produced to be used for carrier purpose in medical applications. Based on our current knowledge of particle toxicology, it is highly desirable that toxicology and technology are linked in this extremely rapid developing area, to learn more about potential risks and also to develop knowledge on the role of surface and size in particle toxicity.
Coal↗
Acute exposure to the abused inhalant, isobutyl nitrite, reduced T cell responsiveness and spleen cellularity.
Isobutyl nitrite is an inhalant abused principally by male homosexuals. We have reported that subchronic inhalation exposure (45 min/day for 14 days) to 900 ppm isobutyl nitrite was immunosuppressive. In the present study, the effects of acute exposure to the inhalant were examined. Mice were exposed in an inhalation chamber to 900 ppm isobutyl nitrite for 45 min. One day later, spleen cellularity was reduced by 39% without selectively depleting CD4(+) or CD8(+) cells. The numbers of peripheral blood leukocytes and peritoneal cells were also reduced. Following acute inhalation exposure, T cell proliferative responses stimulated with allogeneic cells or anti-CD3 and anti-CD28 antibodies were inhibited, while mitogen-induced responses were not affected. Purified T cells exposed to the inhalant also had compromised responses, suggesting a direct effect on T cells. However, the cumulative effects of multiple exposures were necessary to inhibit T-dependent antibody responses or T cell or macrophage cytotoxicity.
Administration, Inhalation↗
Inhibition of specific IgE responses in mice by pre-exposure to inhaled antigen.
Exposure of mice to aerosolized ovalbumin (OA) once weekly for 5 min, or once weekly to 10 microgram OA in PBS intranasally, elicited transient IgE responses which declined by the seventh week. When these animals were challenged intraperitoneally (i.p.) with soluble or alum-precipitated OA, their subsequent IgE responses were markedly suppressed relative to controls. In contrast, i.p. challenge provoked hemaagglutinating antibody (HA) responses to OA in the same animals which were considerably more vigorous than in controls. Adoptive transfer experiments employing splenocytes from mice repeatedly exposed to OA via the respiratory tract revealed the presence of suppressor cells active against OA-specific IgE but not HA responses. Radiotracer studies employing 125I-OA, administered intranasally and by aerosol, indicated that much of the antigen rapidly became associated with the gut.
Animals↗
Effects of repeated in vivo inhalant nitrite exposure on gene expression in mouse liver and lungs.
Exposure to inhalant organic nitrites (drugs of abuse commonly known as "poppers") has been reported to enhance tumor growth in mice, but the mechanism is not fully defined. This study examined the effect of repeated in vivo nitrite exposures on gene expression in the mouse liver and lungs using a gene array panel of 94 cancer- and angiogenesis-related genes. Using 2-fold change as a threshold criterion, repeated nitrite exposure was found to alter the expression of 65 and 23 genes in the liver and lungs, respectively. Six genes were significantly upregulated (p<or=0.05), viz., those encoding VEGF, VEGFD (vascular endothelial growth factor A and D, respectively) in the lungs and FGF1, FGF4 (fibroblast growth factor 1 and 4, respectively), Hsp70 (heat shock 70kDa protein 4), and PF4 (platelet factor 4) in the liver. mRNA encoding HO-1 (heme oxygenase-1) and Smad7 were marginally (p=0.057) stimulated in the liver. Follow-up studies in the liver revealed significant nitrite-induced expression of VEGF protein and mRNA. Immuno-staining of liver slices revealed that the increased hepatic VEGF expression resided mainly in hepatocytes. Stimulation of hepatic VEGF expression by ISBN was not different in endothelial nitric oxide synthase (eNOS) knockout vs. wild-type mice. In conclusion, multiple exposures to inhalant nitrite appeared to cause alteration in the expression of a number of genes relating to cancer and angiogenesis, including VEGF. eNOS presence did not appear to be essential for nitrite-induced VEGF expression. These studies demonstrate that in vivo exposure to inhalant nitrites results in changes in the angiogenesis cascade.
Administration, Inhalation↗
Oxidative DNA damage and defence gene expression in the mouse lung after short-term exposure to diesel exhaust particles by inhalation.
Exposure to diesel exhaust particles (DEP) is suspected to contribute to lung cancer and cardiopulmonary diseases. In recent years generation of reactive oxygen species capable of inducing cellular oxidative stress has been in focus as one of the underlying mechanisms behind the genotoxic effects of particles. However, the role of the antioxidative defence system still needs to be clarified, especially in relation to low-dose DEP exposures. The aim of this study was to characterize the effects of short-term exposure to DEP in terms of DNA damage and expression of key response genes towards oxidative stress in lungs of mice. Mice were exposed by inhalation to 20 or 80 mg/m3 DEP inhaled as either a single dose, or four lower doses (5 and 20 mg/m3) inhaled on four consecutive days. Our results indicate that HO-1 mRNA expression in lung tissue was up-regulated after both types of DEP exposures, whereas OGG1 expression was only up-regulated after repeated exposures. The level of oxidative DNA damage in terms of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) was increased in the lung tissue after a single exposure, whereas increased levels of DNA strand breaks was observed in bronchoalveolar lavage cells after repeated DEP exposures. The levels of 8-oxodG and OGG1 mRNA in lung tissue were mirror images. This suggests that after repeated exposures, up-regulation of DNA repair counteracts an increased rate of 8-oxodG formation leaving the steady state level of 8-oxodG in DNA unchanged. In conclusion, this study indicates that a single high dose of DEP generates 8-oxodG in lung tissue, whereas the same dose inhaled as four low-exposures may up-regulate the antioxidative defence system and protect against generation of 8-oxodG.
Animals↗
Dermal exposure to jet fuel JP-8 significantly contributes to the production of urinary naphthols in fuel-cell maintenance workers.
Jet propulsion fuel 8 (JP-8) is the major jet fuel used worldwide and has been recognized as a major source of chemical exposure, both inhalation and dermal, for fuel-cell maintenance workers. We investigated the contributions of dermal and inhalation exposure to JP-8 to the total body dose of U.S. Air Force fuel-cell maintenance workers using naphthalene as a surrogate for JP-8 exposure. Dermal, breathing zone, and exhaled breath measurements of naphthalene were obtained using tape-strip sampling, passive monitoring, and glass bulbs, respectively. Levels of urinary 1- and 2-naphthols were determined in urine samples and used as biomarkers of JP-8 exposure. Multiple linear regression analyses were conducted to investigate the relative contributions of dermal and inhalation exposure to JP-8, and demographic and work-related covariates, to the levels of urinary naphthols. Our results show that both inhalation exposure and smoking significantly contributed to urinary 1-naphthol levels. The contribution of dermal exposure was significantly associated with levels of urinary 2-naphthol but not with urinary 1-naphthol among fuel-cell maintenance workers who wore supplied-air respirators. We conclude that dermal exposure to JP-8 significantly contributes to the systemic dose and affects the levels of urinary naphthalene metabolites. Future work on dermal xenobiotic metabolism and toxicokinetic studies are warranted in order to gain additional knowledge on naphthalene metabolism in the skin and the contribution to systemic exposure.
Administration, Cutaneous↗