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PubMed1985

Functional and morphologic changes in the lungs of guinea pigs exposed to freshly generated ultrafine zinc oxide.

Guinea pigs were exposed by nose only for 3 hr/day for 6 days to freshly formed zinc oxide (ZnO) particles (projected area diameter = 0.05 micron, sigma g = 2.0) at 5 mg/m3, the currently recommended threshold limit value (TLV). Ventilation, lung mechanics, lung volumes, and diffusing capacity for carbon monoxide (DLCO) in anesthetized, tracheostomized animals at 1, 24, 48, or 72 hr after the end of the last exposure were evaluated. At the same time intervals lung weight, lung fluid content, respiratory epithelial permeability to horseradish peroxidase, gross and microscopic appearance, and [3H]thymidine labeling of nuclei of bronchial and bronchiolar epithelial cells in other groups of animals were measured. Vital capacity, functional residual capacity, alveolar volume, and DLCO were all decreased following the last exposure and did not return to normal values by 72 hr. Increases in flow resistance and decreases in compliance and total lung capacity returned to normal by 72 hr. Lung weights were elevated due to inflammation involving the proximal portion of the alveolar ducts and adjacent alveoli. These changes were still present at 72 hr. [3H]Thymidine labeling of bronchiolar epithelial cell nuclei was increased for 48 hr. Respiratory epithelial permeability to horseradish peroxidase was not affected by the exposures. These results suggest that the current TLV for ZnO may not be adequate.

Animals↗
PubMed1987

Effects of inhalation of ethylene dichloride on pulmonary defenses of mice and rats.

The effects of single or multiple inhalation exposures to ethylene dichloride (DCE) on the pulmonary defense systems of mice and rats were evaluated. Single exposures of mice to the threshold limit value of DCE (10 ppm) resulted in decreased pulmonary bactericidal activity to inhaled Klebsiella pneumoniae and increased mortality from Streptococcus zooepidemicus respiratory infection. A single exposure to 5 ppm DCE caused increased mortality from streptococcal pneumonia although bactericidal activity was not affected. Neither of these two parameters changed following single or five consecutive daily exposures to 2.5 ppm DCE. Single exposures to 10 or 100 ppm DCE did not affect mouse alveolar macrophage (AM) inhibition of the proliferation of a tumor target cell in vitro or AM in vitro phagocytosis of red blood cells. In rats, no effects were observed on pulmonary bactericidal activity. AM in vitro phagocytosis, AM cytostasis and cytolysis of tumor target cells, AM ectoenzymes, or blastogenesis of mitogen-stimulated rat T- and B-lymphocytes from lung-associated, mesenteric, and popliteal lymph nodes following single exposure to 100 or 200 ppm DCE or after twelve 5-hr exposures to 10, 20, 50, or 100 ppm DCE.

Administration, Inhalation↗
PubMed1994

Volatile organic compounds from household waste.

Ninety volatile organic compounds were identified in the headspace of biodegradable and mixed household waste by GC/MS. Most of them could be attributed to biological waste, microbiological growth in biological waste or packaging materials. Although none of the compounds were present at concentrations exceeding their threshold limit values, it is possible that in closed garbage cans or containers organic sulfur compounds could contribute to the reported gastrointestinal problems of collection personnel.

Biodegradation, Environmental↗
PubMed1986

Mercury vapour levels in a domestic environment following breakage of a clinical thermometer.

Following the breakage of a clinical thermometer in the kitchen of the author's own home, mercury vapour was found to be present in most rooms, but not in concentrations which exceeded the current threshold limit value (TLV). However, assuming a more stringent standard of safety, based on continuous exposure to mercury vapour, it was noted that some of the readings could be considered to be excessive, although these were of a freakish and transient nature. In reality the overall time-weighted average exposure of the occupants was within reasonable limits. Lack of ventilation was a major factor in maintaining discernible levels of vapour over a 3-week period. However, the advent of mild weather was instrumental in dispersing the vapour, by allowing the opening of windows. The residual mercury on the floors would seem to have evaporated, so that no long-term health risk ensued. Cross contamination of the hallway carpet was noted indicating that mercury had been transported on the soles of feet and shoes.

Accidents, Home↗
PubMed1988

Element concentrations in the air of an indoor shooting range.

Elemental emissions during firing in a shooting range were measured for different types of ammunition. When using Hirtenberger bullets, lead, barium, antimony and to a lesser extent copper and arsenic were the primary metal pollutants. Stationary sampling at three locations in the range did not reveal large concentration gradients. Large concentration variations were observed by sampling before, during and after shooting. Lead and antimony concentrations peak at 5060 and 119 micrograms m-3, respectively. Soil elements such as aluminium, sodium and calcium are enriched during shooting, probably due to soil resuspension by the shooters and the bullets hitting the sand backstop. After shooting has ceased the concentrations fall to within pre-shooting levels within a couple of hours. Measurement of the aerodynamic particle size shows low mass median diameters for the elements emitted during firing and larger diameters for the soil-associated elements. The peak airborne concentrations measured by stationary sampling, and human exposure measured by a personal sampler carried by an instructor were compared with threshold limit values. During the shooting the TLV is significantly exceeded for lead.

Air↗
PubMed1991

Implications of the Labrador Dust Study.

Joint medical and technical investigations of an iron ore mining and processing operation, over a 2 year period, has confirmed the presence of pneumoconiosis associated with respirable dust exposure above recognized threshold limit values. This study achieved short-term objectives in quantifying dust levels and the extent of pneumoconiosis, and in identifying the need for revised surveillance programs. Definitive conclusions on a variety of dust-related questions are possible by correlating the baseline data generated with a continuous monitoring program.

Adult↗
PubMed1979

Effects of acetone, methyl ethyl ketone and methyl isobutyl ketone on a match-to-sample task in the baboon.

Acetone, methyl ethyl ketone (MEK) and methyl isobutyl ketone (MIBK) were evaluated for effects on a delayed match-to-sample discrimination task in the juvenile baboon. The animals were exposed to 1/2 the threshold limit value (TLV) of each gas for 24 hr per day during a 7-day period. They were also exposed to a combination of MEK and MIBK at the same exposure concentrations. Each exposure condition affected accuracy of performance minimally but resulted in increased and decreased extra responses during the delay intervals. Response times were slowed under acetone, MEK or MIBK. In contrast to the effects of the individual gases, exposure to a combination of the same doses of MEK and MIBK produced a consistent increase in extra responses during delay and a concomitant decrease in response times. Changes in tissue uptake and metabolism are suggested as possible mechanisms to explain this observation.

Acetone↗
PubMed1976

Toluene diisocyanate (TDI) pulmonary disease: immunologic and inhalation challenge studies.

Clinical and serologic effects of TDI exposure were studied in 112 occupationally exposed plant workers. Sera were obtained before and after commencement of TDI production. All subjects were skin-tested with common inhalant allergens and a TDI-HSA conjugate. Total eosinophil counts, immunoglobulin quantitations, and specific antibody assays by PCA, P-K, and radioimmunoassay were performed. Clinically "sensitive" individuals were tested by provocative inhalation challenge with from 0.005 ppm to the threshold limit value of 0.02 ppm TDI. No TDI-induced immunologic changes were noted with the exception of 3 individuals who demonstrated small positive wheal-and-erythema reactions to TDI-HSA but not to HSA alone. Inhalation challenge with TDI vapor produced airways obstruction, as measured by FEF (25-75). These responses were of the immediate, delayed, and dual type, and were provoked in some cases with levels as low as 0.005 ppm TDI.

Airway Obstruction↗
PubMed1994

Induction of type I hypersensitivity in guinea pigs after inhalation of phthalic anhydride.

Guinea pigs were exposed through inhalation to phthalic anhydride (PA) dust at 0.5, 1.0, and 5.0 mg/m3, 3 hours/day for 5 consecutive days. Inhalation challenge with aerosolized phthalic anhydride-guinea pig serum albumin (PA-GPSA) conjugate elicited immediate-onset respiratory reactions in animals exposed to all three levels of dust. Inhalation challenge of a subgroup of animals with phthalic anhydride dust did not elicit an immediate response, as measured by changes in respiratory frequency and plethysmograph pressure. Serologic studies showed that these animals had allergic IgG1a antibody to PA-GPSA. There was a dose-dependent increase in specific IgG antibody activity, as measured by ELISA. Animals exposed to and challenged with 5.0 mg/m3 PA dust had significant numbers of hemorrhagic lung foci. Those animals with the greatest number of foci had high IgG antibody activity to PA, as measured by ELISA. This study showed that exposure to levels of PA dust as low as 0.5 mg/m3, below the current threshold limit value of 6.0 mg/m3, can sensitize animals to produce allergic antibody.

Administration, Inhalation↗
PubMed1986

Curing efficiency and ocular hazards of dental photopolymerization sources.

The spectral distributions of a range of dental photocuring sources were measured at the exit window and at a distance of 10 cm. The former enabled the evaluation of a newly proposed photocuring efficiency index which correlates well with the depth of cure of the photopolymerized resins, thus providing a basis for the comparison of different photocuring sources. The spectral irradiance of the sources obeyed the inverse-square law, allowing a comparison with the ACGIH threshold limit values. According to these criteria, no ocular hazard is posed to the patient or clinician by u.v.-A or u.v.-B radiation nor to the patient by the visible light when momentarily exposed to the sources. Similarly the ACGIH criterion indicates that the clinician does not risk chorioretinal injury provided the exposure is restricted to less than 140 s in a 3 h period.

Acrylic Resins↗
PubMed1985

An experimental design for the simulation of combined-acting pollutants.

A short review is given of concepts which are used to evaluate effects from combined-acting agents. To explore those effects exactly a high multiplicity of experiments must be performed, as an algebraic derivation from the effects of the single-acting agents is not usually possible. For practical purposes (as, for instance, to establish threshold limit values with respect to occupational health standards) a more pragmatic concept is proposed. Accordingly, an experimental setup has been developed which enables us to expose four groups of rodents simultaneously to two different single-acting chemical and/or physical stress parameters, both separately and in combination, and to control conditions.

Air Pollutants↗
PubMed1980

Chromosomal analyses in vinyl chloride exposed workers. Results from analysis 18 and 42 months after an initial sampling.

In a previous study (Purchase et al., Mutation Res., 57 (1978) 325-334) it was reported that 57 workers occupationally exposed to vinyl chloride had an increase in the incidence of chromosomal abnormalities in their lymphocytes by comparison with 24 control workers. Since that time (July 1974) threshold limit values for vinyl chloride and plant exposure levels have been reduced. In the present study, 2 further samples from the same population of workers have been analysed for chromosomal aberrations 18 and 42 months after the initial sampling. At 18 months, 21 VC workers and 6 on-site controls were investigated as were 23 workers and 8 on-site controls at 42 months. In the second sampling there was a tendency to an increase in chromosomal abnormalities of VC-exposed workers except in those people who had changed occupation. By the third sampling, however, there was a decrease by comparison with previous samplings and the levels of abnormalities had returned to values similar to those of the controls. Thus, reduction in exposure to vinyl chloride is accompanied by a reduction in the chromosomal abnormalities to levels indistinguishabe from those of controls.

Adult↗
PubMed1985

The toxicity of dimethylamine in F-344 rats and B6C3F1 mice following a 1-year inhalation exposure.

Dimethylamine is a widely used commodity chemical, for which there are few chronic toxicity data. Male and female F-344 rats and B6C3F1 mice were exposed by inhalation to 0, 10, 50, or 175 ppm dimethylamine (DMA) for 6 hr/day, 5 days/week for 12 months. Groups of 9-10 male and female rats and mice were necropsied after 6 and 12 months of exposure. No male mice were sacrificed at 12 months due to a high incidence of early deaths in that group. The mean body weight gain of rats and mice exposed to 175 ppm DMA was depressed to approximately 90% of control after 3 weeks of exposure. The only other treatment-related changes were concentration-related lesions in the nasal passages. Two distinct locations in the nose were affected: the respiratory epithelium in the anterior nasal passages, and the olfactory epithelium, especially that lining the anterior dorsal meatus. There was focal destruction of the anterior nasoturbinate and nasal septum, local inflammation, and focal squamous metaplasia of the respiratory epithelium in rats and mice. Mild goblet cell hyperplasia was observed only in rats. The olfactory epithelium exhibited extensive loss of sensory cells with less damage to sustentacular cells. There was also loss of olfactory nerves, hypertrophy of Bowman's glands, and distension of the ducts of these glands by serocellular debris in regions underlying degenerating olfactory epithelium. At the 175-ppm exposure level, rats had more extensive olfactory lesions than mice, with hyperplasia of small basophilic cells adjacent to the basement membrane being present in rats but not mice. After 12 months of exposure to 10 ppm DMA, minimal loss of olfactory sensory cells and their axons in olfactory nerve bundles was observed in the nasal passages of a few rats and mice. These results indicate that the olfactory sensory cell is highly sensitive to the toxic effects of DMA, with minor lesions being produced in rodents even at the current threshold limit value of 10 ppm.

Air Pollutants↗
PubMed1985

Immunotoxicologic evaluation of the respiratory system: animal models for immediate- and delayed-onset pulmonary hypersensitivity.

A wide variety of industrial materials is known to cause allergic pulmonary reactions. Respiratory symptoms may occur either immediately upon exposure to the agent (immediate-onset response), or several hours later (delayed-onset reaction). In order to determine both the mechanism of response, and a safe exposure level which would prevent development of pulmonary sensitization, animal models are currently being developed for both types of sensitivity responses. In the models, emphasis is placed on simulating conditions present in the industrial environment. For example, (1) exposure to agents is via the inhalation route, (2) animals are unrestrained and unanesthetized both during exposure and during elicitation of response, and (3) reactive chemicals, as opposed to hapten-protein conjugates, are used for exposure. In the model for immediate-onset sensitivity, concentration-response relationships have been observed between the concentration of agent inhaled and the percentage of animals becoming sensitized. Agents employed were bacterial subtilisin and toluene diisocyanate. Identification of "no observable effect" threshold concentrations implies that exposure levels can be proposed for industrial chemicals which will not result in sensitization of workers. Further development of the animal models, followed by calibration of the models to humans, should allow immunotoxicologic evaluation of chemicals for their respiratory sensitizing ability and recommendation of threshold-limit values (TLVs) which would prevent sensitization.

Animals↗
PubMed1986

Methyl isocyanate subchronic vapor inhalation studies with Fischer 344 rats.

Groups of Fischer 344 rats were exposed to 3.1, 0.6, 0.15, or 0.0 (control) ppm of methyl isocyanate (MIC) vapor 6 hr per day for two 4-day sessions separated by a 2-day rest. There were no deaths during the study. The rats were killed the morning following the last exposure day. The 3.1-ppm-exposed rats had decreased body weight, food consumption, and blood oxygen saturation (males only). Increased hemoglobin concentration (males only) and lung weights were also observed in this group of rats. Multiple histologic lesions, limited to the respiratory tract, were observed in rats of the 3.1-ppm group only. The lesions consisted of necrosis, suppurative inflammation, squamous metaplasia, and intraluminal and submucosal fibroplasia (bronchi and bronchioles only) which extended from the anterior nasal cavity to the terminal bronchioles. In a second study, rats were exposed to 3.0 ppm MIC, 6 hr per day, for either one or two 4-day sessions and sacrificed on postexposure Days 1, 15, 43, and 85. All rats survived the 4- or 8-day exposure regimen, although significant decreases in body weight and encrustation of the eyes, nose, or mouth area were observed. During the first 15 days postexposure, male mortality was 63%; only 6% of the MIC-exposed females died. The cause of death was interpreted to be a combination of pulmonary vascular and inflammatory changes coupled with anorexia. For survivors, recovery from the necrotizing and irritating effects of MIC vapor was observed. Squamous metaplasia of respiratory epithelium, observed in rats sacrificed at the end of the exposure period, was replaced by tall pseudostratified columnar (regenerative) epithelium beginning in the bronchi and bronchioles as well as the distal trachea. Collagen maturation and condensation of the intraluminal and submucosal fibroplasia occurred during the postexposure period. The results of these investigations support the current threshold limit value for MIC of 0.02 ppm.

Administration, Inhalation↗
PubMed1986

The effects of inhalation of organic chemical air contaminants on murine lung host defenses.

The potential health hazards of exposure to threshold limit value (TLV) concentrations of acetaldehyde, acrolein, propylene oxide, chloroform, methyl chloroform, carbon tetrachloride, allyl chloride, methylene chloride, ethylene trichloride, perchloroethylene, benzene, phenol, monochlorobenzene, and benzyl chloride, compounds which may be present in the ambient or work room atmosphere were investigated. The effects of single and multiple 3-hr inhalation exposures were evaluated in mice by monitoring changes in their susceptibility to experimentally induced streptococcus aerosol infection and pulmonary bactericidal activity to inhaled Klebsiella pneumoniae. When significant changes in these parameters were found, further exposures were performed at reduced vapor concentrations until the no-measurable-effect level was reached. Multiple exposures on 5 consecutive days were then performed at this concentration. Significant increases in susceptibility to respiratory streptococcus infection were observed after single 3-hr exposure to TLV concentrations of methylene chloride, perchloroethylene, and ethylene trichloride. For methylene chloride and perchloroethylene, these exposure conditions also resulted in significantly decreased pulmonary bactericidal activity.

Air Pollutants↗
PubMed1987

Comparative inhalation toxicity of nickel subsulfide to F344/N rats and B6C3F1 mice exposed for 12 days.

Groups of F344/N rats and B6C3F1 mice were exposed to aerosols of nickel subsulfide (Ni3S2) 6 hr/day for 12 days not including weekends. Actual exposure concentrations were within 3% of target (target = 10.0, 5.0, 2.5, 1.2, 0.6, and 0.0 mg Ni3S2/m3). Nickel lung burdens of exposed rats and mice increased linearly with exposure concentration. Two male rats and all mice exposed to 10.0 mg Ni3S2/m3 died before the end of the exposures. Exposure to Ni3S2 had no effect on the natural killer cell activity of mouse spleen cells. Lesions in rats and mice related to inhalation of Ni3S2 were found in the nasal epithelium, lung, and bronchial lymph nodes. The most extensive lesions were found in the lung and included necrotizing pneumonia. Emphysema developed in rats exposed to 5.0 or 10.0 mg Ni3S2/m3, while fibrosis developed in mice exposed to 5.0 mg Ni3S2/m3. Degeneration of the respiratory epithelium and atrophy of the olfactory epithelium of the nose occurred in rats exposed to as low as 0.6 mg Ni3S2/m3 and mice exposed to 1.2 mg/m3. Results indicate that inhalation exposure of rats and mice to Ni3S2 aerosol concentrations near the current threshold limit value (TLV) for nickel compounds (1 mg/m3 for Ni metal and roasting fume and dust and 0.1 mg/m3 as Ni for soluble compounds) can produce lesions in the respiratory tract. Atrophy of lymphoid tissues (spleen, thymus, and bronchial lymph nodes) was found in animals of the highest exposure concentration. Degeneration of the testicular germinal epithelium was also observed in mice and rats that survived 5.0 or 10.0 mg/m3 exposure concentrations.

Animals↗
PubMed1988

Comparative inhalation toxicity of nickel sulfate to F344/N rats and B6C3F1 mice exposed for twelve days.

Groups of F344/N rats and B6C3F1 mice were exposed to aerosols of nickel sulfate hexahydrate (NiSO4.6H2O) 6 hr/day for 12 days to determine the short-term inhalation toxicity of this compound. Target exposure concentrations were 60, 30, 15, 7, 3.5, and 0 mg NiSO4.6H2O/m3. Endpoints evaluated included clinical signs, mortality, quantities of Ni in selected tissues, effect on mouse resistance to tumor cells, and pathological changes in tissues of both rats and mice. All mice exposed to 7 mg NiSO4.6H2O/m3 or greater and 10 rats exposed to 15 mg NiSO4.6H2O/m3 or greater died before the termination of exposures. Quantities of Ni remaining in lungs of rats at the end of the exposure were independent of exposure concentration. Lung burdens of Ni in mice were approximately one-half that in lungs of rats. Exposure of female mice to 3.5 mg NiSO4.6H2O/m3 had no effect on resistance to tumor cells as determined by spleen natural killer cell activity. Histopathological changes were seen in tissues of rats and mice exposed to as low as 3.5 mg NiSO4.6H2O/m3. Lesions related to NiSO4.6H2O exposure occurred in lung, nose, and bronchial and mediastinal lymph nodes. Results indicated that exposure of rats and mice to amounts of NiSO4.6H2O aerosols resulting in Ni exposure concentrations only eight times greater than the current threshold limit value for soluble Ni (0.1 mg/m3) for as little as 12 days can cause significant lesions of the respiratory tract.

Administration, Inhalation↗