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PubMed1990

Uptake, distribution and elimination of alpha-pinene in man after exposure by inhalation.

The toxicokinetics of alpha-pinene were studied in human volunteers exposed by inhalation (2 h, 50 W) in an exposure chamber on four occasions. The exposures were about 10, 225, and 450 mg/m3 (+)-alpha-pinene and 450 mg/m3 (-)-alpha-pinene. The relative pulmonary uptake was about 60% for the higher exposures, and total uptake increased linearly with increasing exposure. The total blood clearance was high, about 1.11.h-1.kg-1. After the exposure was terminated, less than 0.001% of the total uptake was eliminated unchanged in the urine and about 8% in exhaled air. A long half-time in poorly perfused tissues indicates a high affinity to adipose tissues. There was a statistically significant exposure-response relationship among five subjects who experienced irritation. Short-time exposure to alpha-pinene did not give rise to acute changes in lung function 20 min after the exposure.

Air Pollutants, Occupational↗
PubMed1997

Grouping strategies for exposure to inhalable dust, wheat allergens and alpha-amylase allergens in bakeries.

This paper describes repeated measurements of inhalable flour dust, wheat allergens and alpha-amylase allergens in the bakery industry. A total of 571 full-shift personal dust samples was collected. Wheat allergens and alpha-amylase allergens were measured in 449 and 507 samples, respectively, by the use of recently developed immunoassays. For all three measures of exposure, the main components of exposure variability were determined. Different grouping strategies for studying exposure-response relationships were compared. The specific job of a bakery worker was identified as the most important source of variability in inhalable flour dust concentrations. For exposure to wheat allergens, the job performed was also the most important source of variation, but type of bakery also explained some of the variability. For alpha-amylase allergen exposure, information on type of bakery was more important then job information. For exposure to inhalable dust and wheat allergens, a classification by job title would lead to sufficient contrast in average exposure levels. By contrast, a grouping strategy based on a combination of job and type of bakery appeared to be essential to obtain a useful classification of exposure to alpha-amylase allergens. 1997 British Occupational Hygiene Society.

Allergens↗
PubMed1994

[The importance of formic acid excretion in the urine for environmental and occupational medicine questions].

The suitability of the formic acid excretion in the urine as a parameter for the biological monitoring of inhalational exposure to formaldehyde is discussed controversially. We investigated persons not occupationally exposed to formaldehyde (n = 70) to determine possible influencing factors on the physiological excretion of formic acid. Following this we carried out a study on medical students (n = 30), who during an anatomical dissection course were exposed to a short but intensive inhalational exposure to formaldehyde, as well as investigations on employees of a pathological-anatomical laboratory (n = 8) in order to observe the course of the formic acid excretion in the urine during a working week with a continuous exposure to formaldehyde below or within the range of the MAK value (0.5 ppm). It was seen that the formic acid excretion in the urine with non-exposed persons is subject to considerable inter and intraindividual fluctuations (at a maximum by a factor of 30). In addition to differences in the endogenous formation of formates an important influencing factor is probably the uptake of food containing formic acid or its precursors. A value of 23 mg formic acid/g creatinine is given as the upper norm level (95th percentile) of adults. In the groups who were exposed to formaldehyde, in some cases considerably above the MAK value, we were able to detect no significant increase in the formic acid concentration in the urine. After a short but intensive exposure to formaldehyde (0.32-3.48 ppm) the formic acid concentration in the urine did not change significantly with an average formic acid concentration in the urine before exposure of 6.5 mg/g creatinine (central 50% range: 3.5-14.2 mg/g creat.) and after exposure of 6.0 mg/g creatinine (central 50% range: 4.4-10.9 mg/g creat.). There was no significant relationship between the individual change in the formic acid concentration in the urine (in mg/g creatinine) and the inhalational exposure to formaldehyde determined through personal air sampling (r = 0.079). In the course of a working week with a continuous exposure to formaldehyde (0.03-0.83 ppm) there was after relating the values to creatinine a continuous increase in the median to 22.3 mg/g creat. with a starting value of 8.7 mg/g creat. The change proved, however, for the number of cases investigated not to be significant. In particular there was no linear correlation detectable between the individual changes in the formic acid excretion in the urine and the formaldehyde concentrations in the breathing zone determined by personal air sampling.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Inhalation↗
PubMed2001

A comparison and critique of historical and current exposure assessment methods for beryllium: implications for evaluating risk of chronic beryllium disease.

The primary beryllium industry has generated a large amount of data on airborne beryllium concentrations that has been used to characterize exposure by task-specific activities, job category, individual worker, and processing area using a variety of methods. These methods have included high-volume breathing zone sampling, high-volume process sampling, high- and low-volume respirable and area sampling, real-time monitoring, and personal sampling. Many of the beryllium studies have used these air sampling methods to assess inhalation exposure and chronic beryllium disease (CBD) risk to beryllium; however, available data do not show a consistent dose-response relationship between airborne concentrations of beryllium and the incidence of CBD. In this article, we describe the air sampling and exposure assessment methods that have been used, review the studies that have estimated worker exposures, discuss the uncertainties associated with the level of beryllium for which these studies have reported an increased risk of CBD, and identify future investigative exposure assessment strategies. Our evaluation indicated that studies of beryllium workers are often not directly comparable because they (1) used a variety of exposure assessment methods that are not necessarily representative of individual worker exposures, (2) rarely considered respirator use, and (3) have not evaluated changes in work practices. It appears that the current exposure metric for beryllium, total beryllium mass, may not be an appropriate measurement to predict the risk of CBD. Other exposure metrics such as mass of respirable particles, chemical form, and particle surface chemistry may be more related to the prevalence of CBD than total mass of airborne beryllium mass. In addition, assessing beryllium exposure by all routes of exposure (e.g., inhalation, dermal uptake, and ingestion) rather than only inhalation exposure in future studies may prove useful.

Air Pollutants, Occupational↗
PubMed1988

The carcinogenicity of discontinuous inhaled benzene exposures in CD-1 and C57Bl/6 mice.

Groups of male C57Bl and CD-1 mice were exposed to benzene via inhalation using two different exposure protocols. One protocol consisted of repetitive week-long exposures to 300 ppm benzene (6 h/d x 5 d/wk) interrupted by 2 weeks of non-exposure. The exposure pattern (1 week of exposure followed by 2 weeks of non-exposure) was continued until the death of the last exposed animal. The second protocol consisted of exposures to 1200 ppm benzene (6 h/d x 5 d/wk) for 10 weeks. Exposures were then terminated and the animals allowed to live out their lives. For each protocol, appropriate age-matched control mice received comparable exposures to filtered, conditioned air. The discontinuous exposure patterns mimic the patterns of exposure often encountered in the workplace and, in addition, prolong the survival of exposed animals so as to maximize potential tumorigenic responses. Both exposure protocols were markedly hematotoxic to both mouse strains as measured by peripheral blood counts. Both strains of mice responded to the intermittent 300 ppm benzene exposures with elevated incidences of malignant tumors. Particularly noteworthy was a 35% incidence of zymbal gland tumors in the C57Bl mice. In contrast, only the CD-1 mice responded to the 1200 ppm benzene exposures delivered over 10 weeks with elevated tumor incidences. A 46% incidence of lung adenoma was particularly striking in these mice. Neither of the benzene exposure protocols induced elevated incidences of leukemia/lymphoma in either strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1994

The toxicity of 1-week exposures to inhaled chloroform in female B6C3F1 mice and male F-344 rats.

Detailed quantitative descriptions of the toxicity of inhaled chloroform are lacking, despite the fact that the majority of environmental exposures occur by this route. We investigated the ability of chloroform vapors to produce toxicity and regenerative cell proliferation in the livers and kidneys, the principal target organs for carcinogenicity of female B6C3F1 mice and male F-344 rats, respectively. Nasal passages were also examined for toxic responses. Rodents were exposed to chloroform vapors at concentrations of 0, 1, 3, 10, 30, 100, or 300 ppm for 6 hr/day for 7 consecutive days and necropsied on Day 8. Animals were administered bromodeoxyuridine (BrdU) via implanted osmotic pump for the previous 3.5 days before necropsy. Cell proliferation was quantitated as the percentage of cells in S-phase (labeling index; LI) measured by immunohistochemical detection of BrdU-labeled nuclei. Mice exposed to 100 or 300 ppm exhibited centrilobular hepatocyte necrosis and severe vacuolar degeneration of midzonal and periportal hepatocytes, while exposure to 10 or 30 ppm resulted in mild to moderate vacuolar changes in centrilobular hepatocytes. Slight, dose-related increases in the hepatocyte LI were observed for exposure concentrations of 10 and 30 ppm, while the LI was increased more than 30-fold in the 100 and 300 ppm groups. The kidneys of mice were affected only at the 300 ppm exposure, with approximately half of the proximal tubules lined by regenerating epithelium and an increased LI of tubule cells of 8-fold over control. In rats, mild centrilobular vacuolation was observed only in the livers of rats exposed to 300 ppm. The hepatocyte LI in rats were increased only at 100 and 300 ppm, 3- and 7-fold over control, respectively. In the kidneys of the male rats exposed to 300 ppm, about 25 to 50% of the proximal tubules were lined by regenerating epithelium. The LI for tubule cells in the cortex was increased at 30 ppm and above. In the nasal passages of rats, chloroform concentrations of 10 ppm and above induced histopathological changes that exhibited clear concentration-related severity. These lesions consisted of respiratory epithelial goblet cell hyperplasia and degeneration of Bowman's glands in olfactory mucosa with an associated osseous hyperplasia of the endo- and ectoturbinates in the periphery of the ethmoid region. These nasal lesions were not observed in mice. Knowledge of the dose-dependent responses in rats and mice will be valuable in assessing the potential risks to humans posed by inhaled chloroform and in setting exposure concentrations for longer-term studies.

Administration, Inhalation↗
PubMed1992

[Chronic exposure to inhalation anesthetics and immunity].

The existence of a professional disease caused by exposure to general anesthetics has been reported by a number of studies, but opinions still differ as to the effective implications of this type of exposure. The aim of the present study was to analyse alterations in cellular and humoral immunity in anesthetists regularly exposed to general anesthetics. Regression analysis showed that IgA and NK lymphocytes were significantly increased whereas total T lymphocytes reduced in parallel with age and length of service. It can therefore be supposed that the increase in IgA might suggest chronic liver disease, while alterations in the lymphocyte populations, even if closely associated to chronic exposure leading to the hypothesis of a cause-and-effect relationship, do not alter immune system functions since they are similar to those that occur with ageing.

Adult↗
PubMed2007

Prolonged inhaled allergen exposure can induce persistent tolerance.

Murine asthma models suggest that failure of immune tolerance rather than a defective T helper cell type 1 (Th1) immunity underlies the immune biology of Th2-driven allergen-induced airway disease. Intriguingly, prolonged exposures can result in a full waning of inflammation. The mechanisms underlying this observation are not understood. We hypothesized that the fading of inflammation is the result of regulatory processes, characterized by altered dendritic cell (DC)-T cell interactions. First, we implemented a model in which mice developed Th2-driven airway disease. When we subjected these mice to prolonged antigen ovalbumin (OVA) exposures (8 wk), all inflammation disappeared. Re-immunization and re-challenge showed an inability to mount Th2-skewed immune responses, with absence of airway eosinophils, IgE, and Th2 cytokines. Besides specific immune tolerance, bystander protection was observed. A decrease in CD4+CD25+Foxp3+ T-regulatory cells, PD-1, and IL-10 expression was discerned as compared with acute inflammation. In addition, suppression of ICOS and CD28 was found, along with inhibited DC maturation. This process of disease inhibition surprisingly had a long-lasting memory and was not caused by endotoxin signaling through TLR-4. In summary, our results indicate that the disappearance of Th2-driven airway disease upon persistent antigen exposure is associated with the induction of immune tolerance. The tolerant state is antigen-dependent, and extends to bystander antigens. Moreover, this tolerance is characterized by an altered DC-T cell communication and is long-lasting. Our data further suggest that the mechanism of the disease inhibition after allergic airway inflammation differs from the anti-inflammatory mechanisms observed during acute eosinophilic airway inflammation.

Allergens↗
PubMedDate not supplied

Inhalation administration of all-trans-retinoic acid for treatment of elastase-induced pulmonary emphysema in Fischer 344 rats.

A past study demonstrated that all-trans-retinoic acid (ATRA) treatment by intraperitoneal injection in a rat model of elastase-induced emphysema caused tissue regeneration as evidenced by a decrease in alveolar size and lung volume and an increase in alveolar number. We postulated that treatment with this retinoid by nose-only inhalation exposure would be a more efficient means of targeting damaged lung tissue. Emphysema was induced in male Fischer 344 rats by intratracheal instillation of pancreatic elastase (0.5 IU/g body weight). Four weeks after elastase instillation, animals were treated once daily, 4 days/week, for 3 weeks by exposing them nose-only to aerosolized ATRA (target concentration-time of 3000 or 15,000 mg-min/m3) or by injecting them intraperitoneally with ATRA in cottonseed oil (0.5 or 2.5 mg/kg). Based on estimates of particle deposition in the respiratory tract, inhalation doses were chosen to be consistent with injected doses. Lungs were fixed by inflation with formalin (constant pressure for 6 hours followed by >48 hours of immersion) and were embedded in paraffin. Sections were evaluated by histopathology and stereology. Inhalation exposure to ATRA at both aerosol concentrations caused significant elevations of ATRA in the lung, whereas only the high-dose injection treatment was associated with an elevation of lung ATRA. The mean ATRA concentration from lungs of rats in the high-dose inhalation exposure groups as measured by liquid chromatography--mass spectrometry was approximately 12-fold greater than that of high-dose injection-treated rats. Elastase instillation caused increased lung volumes, irregular alveolar air space enlargement, and fragmentation and attenuation of alveolar septa. Neither inhaled nor injected ATRA reduced the enlarged lung volumes associated with this emphysema model. Stereology demonstrated that alveolar air space enlargement in ATRA-treated rats was similar to that in sham-treated emphysematous animals. Thus, while inhalation treatment caused greater levels of the drug in lung tissue in comparison to that of injection-treated animals, treatment with ATRA by either route of administration did not cause a reversal of lung tissue damage in this model of elastase-induced emphysema.

Administration, Inhalation↗
PubMed1981

Morphologic changes in mouse spermatozoa after exposure to inhalational anesthetics during early spermatogenesis.

The authors studied anesthetic mutagenesis following exposure in vivo by use of an adaptation of the mouse spermatozoa morphology assay of Wyrobek and Bruce. The epididymal spermatozoa of (C57B1/C3H)F1 mice were examined for morphologic abnormalities following exposure to near-0.1 MAC and greater concentrations of general anesthetics. Twenty exposure hours (4 hr/day x 5 days) were conducted for nitrous oxide, diethyl ether, chloroform, trichlorethylene, halothane, methoxyflurane, enflurane, and isoflurane, each at two concentrations. Twenty-eight days after exposure, epididymal spermatozoa were examined. Statistically significant increases in the percentages of abnormal spermatozoa were found for chloroform, trichloroethylene, and enflurane, compared with controls. These data suggest that direct examination of reproductive cells following exposure to general anesthetics in vivo may be useful in the investigation of the genetic toxicities of these compounds.

Anesthetics↗
PubMed1996

Acute inhalation toxicity testing: considerations of technical and regulatory aspects.

The EU regulatory statute for the acute hazard identification of chemicals requires selection of the two most appropriate routes of administration. Testing employing the oral route is mandatory, whereas selection of the dermal or inhalation route requires expert judgement, i.e. considerations of structural alerts with regard to the inherent acute inhalation toxicity as well as the likelihood of dermal and inhalation exposure, respectively. Currently, testing of chemicals requires acute inhalation exposure of 4-h and 1-h durations according the EU classification and labelling and UN Transport Guidelines, respectively. The analysis made revealed that 1-h exposures appear to add little knowledge in addition to existing 4-h LC50 values and a default value of 4 should be used for conversion of 4-h to 1-h LC50 values, independently of the physical state of the chemical. Therefore, also the unit of concentration of exposure atmospheres should be independent of nominal features of the test substance. Hence, the preferred dose metric is mass (mg/liter air) rather than volume (ppm). Taking into account the overall variability of acute toxicity data the recommendations given are classification into the following groups of 4-h LC50 values: < or = 0.05, > 0.05-0.2, > 0.2-1, > 1-5 and > 5.0 mg/l. No distinction should be made concerning vapours and aerosols with regard to units and conversion factors from 4-h to 1-h LC50 values and the default factor of 4 appears to be most suitable. Further differentiation of classification is not indicated due to technical variability of acute inhalation testing and resolution of the acute bioassay.

Administration, Inhalation↗
PubMed1988

Development of a rodent lung macrophage chromosome aberration assay.

Lung macrophages are the first line of defense against inhaled xenobiotics. They are able to accumulate airborne particulates as well as having metabolic capability. They may thus be sensitive indicator cells for detecting inhalation exposure to environmental mutagens. Their usefulness as a short-term in vivo genotoxic assay has not, however, been adequately explored. We have systematically investigated the feasibility of developing a lung macrophage chromosome-aberration assay. It was found that with different types of spindle-binding chemicals (vinblastine and vincristine), and with improved harvesting procedures, an adequate number of metaphase cells can be collected from mice and Chinese hamsters. The chromosome aberration frequencies in macrophages from control mice and Chinese hamsters were found to be 1.2 +/- 2.3 and 0.75 +/- 2.2 per 100 cells respectively. These frequencies are within normal ranges for other somatic cells. After inhalation exposure to an occupational-exposure level of benzene (0, 0.1 and 1 ppm), significant dose-dependent induction of aberrations (1.2 +/- 2.3, 5.7 +/- 6.3 and 6.8 +/- 6.2 chromatid deletions per 100 cells resp.) were observed in the macrophages. Thus, these cells can be used as one of a battery of in vivo assays for inhalation exposure studies.

Animals↗
PubMed2002

Respiratory carcinogenicity assessment of soluble nickel compounds.

The many chemical forms of nickel differ in physicochemical properties and biological effects. Health assessments for each main category of nickel species are needed. The carcinogenicity assessment of water-soluble nickel compounds has proven particularly difficult. Epidemiologic evidence indicates an association between inhalation exposures to nickel refinery dust containing soluble nickel compounds and increased risk of respiratory cancers. However, the nature of this association is unclear because of limitations of the exposure data, inconsistent results across cohorts, and the presence of mixed exposures to water-insoluble nickel compounds and other confounders that are known or suspected carcinogens. Moreover, well-conducted animal inhalation studies, where exposures were solely to soluble nickel, failed to demonstrate a carcinogenic potential. Similar negative results were seen in animal oral studies. A model exists that relates respiratory carcinogenic potential to the bioavailability of nickel ion at nuclear sites within respiratory target cells. This model helps reconcile human, animal, and mechanistic data for soluble nickel compounds. For inhalation exposures, the predicted lack of bioavailability of nickel ion at target sites suggests that water-soluble nickel compounds, by themselves, will not be complete human carcinogens. However, if inhaled at concentrations high enough to induce chronic lung inflammation, these compounds may enhance carcinogenic risks associated with inhalation exposure to other substances. Overall, the weight of evidence indicates that inhalation exposure to soluble nickel alone will not cause cancer; moreover, if exposures are kept below levels that cause chronic respiratory toxicity, any possible tumor-enhancing effects (particularly in smokers) would be avoided.

Animals↗
PubMed1998

[Laughing gas as the principle substance in assessing occupational exposure to inhalation anesthetics].

PURPOSE: In the Federal Republic of Germany limits for the chronic exposure to nitrous oxide and volatile anaesthetics have been prescribed by legislation. According to the technical rules for the handling of hazardous substances TRGS 402 it is legal to measure a single substance in a mixture of hazards, unless the behaviour of all substances is known. Studies about corresponding concentrations of nitrous oxide and volatile anaesthetics in anaesthetic working areas have not yet been carried out. METHODS: During one working week each the concentrations of nitrous oxide, enflurane and desflurane were measured by infrared spectrometry in a working area equipped with air condition and in a non-ventilated operating theatre. Corresponding concentrations of nitrous oxide were measured from the same gas samples. RESULTS: Statistical calculations showed linear correlations of the enflurane and nitrous oxide concentrations in all anaesthetic areas. No linear regression was found between the desflurane and nitrous oxide concentrations. In the working area where desflurane anaesthesias were carried out, significantly higher concentrations of nitrous oxide were observed. Nevertheless the Chi2-test showed no significant differences in the distribution of categorised measurement values. DISCUSSION: Although it is not possible to calculate desflurane concentrations from the nitrous oxide concentrations, measurement of nitrous oxide as leading substance is a valid procedure to assess the exposure of the anaesthesiology workplace to nitrous oxide and volatile anaesthetics. Significant higher nitrous oxide concentrations during desflurane anaesthesia result from early extubation of patients expiring higher concentrations of nitrous oxide.

Air Pollution, Indoor↗
PubMed1991

[Irreversible changes in energy processes in the mitochondria after chronic exposure to detergents].

Chronic inhalational exposure of white rats to a synthetic detergent 'LOTOS' in concentrations 25 and 100 mg/m3 caused liver mitochondria bioenergetics changes from a reversible low energetic shift up to an irreversible mitochondria damage of an organ-structural character. The degree of the damaging effect depended on the duration of exposure and the concentration of the detergent.

Administration, Inhalation↗
PubMed1998

The effect of of glucocorticoids on grain dust-induced airway disease.

STUDY OBJECTIVES: To determine the effect of glucocorticoids on grain dust-induced airflow obstruction and airway inflammation. DESIGN: Randomized controlled trial. SETTING: University hospital. PARTICIPANTS: Health volunteers. INTERVENTIONS: Two randomized, placebo-controlled trials, each studying 10 healthy volunteers who were pretreated with either triamcinolone acetonide (Azmacort) oral inhaler 4 puffs twice daily (800 microg daily) for 7 consecutive days or IV hydrocortisone (3 microg/kg/min) as a 14-h continuous infusion, then subjected to a controlled inhalation exposure to corn dust extract (CDE) (endotoxin exposure dose of 3 microg/kg). A single-blind, crossover study design was performed for each trial enrolling 10 healthy, lifetime nonsmokers, with no history of lung disease or environmental exposure to grain dust. MEASUREMENTS AND RESULTS: Following each inhalation exposure to CDE, spirometry was performed at regular intervals and BAL was performed at 4 h. Both treatment and placebo groups demonstrated significant decrements in spirometry and increments in BAL cellularity following CDE inhalation compared with placebo. Inhaled steroid treatment resulted in a significantly higher FEV1 only at the 2-h time point following CDE inhalation with no significant differences observed in the BAL total cell concentration or cellular differential compared with placebo. IV hydrocortisone treatment resulted in a significantly higher FEV1 and FVC between 2 and 4 h after CDE inhalation, as well as significant reductions in the BAL total cell, macrophage, and eosinophil concentrations. Interestingly, the concentration of tumor necrosis factor-alpha and interleukin-8 in the BAL fluid was also decreased following treatment with IV glucocorticoids. CONCLUSIONS: These results demonstrate that glucocorticoids, administered IV and perhaps by inhalation, have a mildly protective effect on airflow obstruction and airway inflammation induced by inhalation of grain dust.

Administration, Inhalation↗