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PubMed1995

Low flow anaesthesia reduces occupational exposure to inhalation anaesthetics. Environmental and biological measurements in operating room personnel.

In the present study we evaluated the occupational exposure to N2O and isoflurane during open circuit (OC) (fresh gas flow > or = minute volume) and low flow (LF) (fresh gas flow = 1.5 l/min) anaesthesia. The effects of active scavenging and of a charcoal filter positioned on the exhausting branch of the ventilator on environmental and urinary concentrations of inhalation anaesthetics were also investigated. The study was carried out in the same operating room provided with non-recirculating air changes (10 per hour). It involved anaesthetists and nurses during routine activity. N2O and isoflurane concentrations (time-weighted average) were measured after 3-hour continuous exposure: 1) in the environment at the level of the personnel's breathing zone (Ci); 2) in the environment at the ventilator zone (C); 3) in urine (Cu). During OC anaesthesia without active scavenging the breathing zone concentration of both N2O and isoflurane was very high (194.6 +/- 15.2 and 5.0 +/- 0.4 ppm, respectively). The activation of the scavenging greatly reduced the breathing zone concentration of N2O (31.6 +/- 4.1 ppm) and isoflurane (1.7 +/- 0.2 ppm). LF anaesthesia (with active scavenging) significantly reduced the environmental concentration of both anaesthetics (Ci N2O and isoflurane 22.7 +/- 1.8 and 0.6 +/- 0.04 ppm, respectively). During LF anaesthesia the breathing zone concentration of N2O remained low, even without scavenging (22.7 +/- 1.8 ppm). Similar results were obtained by measuring N2O and isoflurane concentrations at the ventilator zone and in urine.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants, Occupational↗
PubMed1993

Relevance of occupational skin exposure.

Dermal exposure gains in significance by the same token as permissible occupational inhalation exposures are lowered. The contribution of dermal absorption to the total dose absorbed during occupational exposure is apparent when dermal and pulmonary uptake rates are compared. Development of an experimental data base for evaluation and control of dermal exposure is hindered by: lack of suitable methods for measurement of dermal absorption in humans; interspecies differences in skin permeability; regional differences in absorption rates due to non-homogeneity of skin composition and perfusion rates over the body; possible skin damage induced by the chemical or dispersant; and exposure conditions in the workplace. In the absence of sufficient human data, theoretical models can provide satisfactory information on dermal absorption. It is advocated that the current practice of using acute dermal toxicity (LD50) as a criterion for warning on the potential of significant dermal absorption be replaced by a criterion based on comparison of the dermal penetration rate with the pulmonary uptake rate at inhalation exposures permissible in the workplace.

Air Pollutants, Occupational↗
PubMed1997

Respiratory irritative effects of trimethylbenzenes: an experimental animal study.

Sensory respiratory irritation effects of trimethylbenzene isomers (TMBs) (hemimellitene, mesitylene and pseudocumene) in male Balb/C mice were investigated in conditions of acute exposure and in male Wistar rats in conditions of repeated 90-day inhalation exposure to pseudocumene. The pseudocumene, mesitylene and hemimellitene concentrations depressing the respiratory rate to 50% (RD50) were 578, 519, 541 ppm, respectively. Inhalation exposure to pseudocumene for 90 days increased the total number of cell macrophages, polymorphonuclear leukocytes and lymphocytes number at all three test concentrations compared with the controls. Total protein lactate dehydrogenase (LDH) and acid phosphatase activity in bronchoalveolar lavage (BAL) were significantly increased in all exposed groups. Based on the effects observed in the respiratory tract, the threshold limit value of at least 10 ppm should be considered for the occupational exposure to trimethylbenzene isomers.

Animals↗
PubMed2003

Assessment of metabolites and AhR and CYP1A1 mRNA expression subsequent to prenatal exposure to inhaled benzo(a)pyrene.

Few studies have focused on environmental aerosol contaminant, mechanistically-based, dose-related neurotoxicity with respect to development of the central nervous system. To fill this important data gap and to highlight possible mechanistic pathways, a study was undertaken to determine metabolite concentrations associated with the transplacental disposition of inhaled benzo(a)pyrene (B(a)P) and the resulting effects on the status of aryl hydrocarbon receptor (AhR), and cytochrome P450 1A1 (CYP1A1) mRNA in preweaning F1 generation animals. In this study, laparotomy on GD 8 was performed on timed-pregnant rats followed by dosing via nose-only exposure for 4h a day for 10 days (GD 11-GD 20) to three concentrations of a B(a)P: carbon black aerosol (25, 75 and 100 microg/m(3)). A dose-dependent decrease in birth index was observed in the B(a)P exposed group as compared to the controls (P<0.05). Analysis of cerebrocortical extracts from F1 generation pups revealed a dose-dependent (P<0.05) increase in total B(a)P metabolites. Analysis of cerebrocortical and hippocampal mRNA developmental expression profiles for AhR and CYP1A1 using 18sRNA as the internal standard, revealed that inhaled B(a)P upregulates AhR during the first postnatal month. The present study suggest that prenatal exposure to inhaled B(a)P upregulates hepatic aryl hydrocarbon receptor dependent mechanisms in the F1 generation. Hepatic upregulation of the aryl hydrocarbon receptor may modulate the potential for benzo(a)pyrene toxicity via the activation of cytochrome P450 and the subsequent deposition of lipophillic metabolites to developing central nervous system structures such as cerebral cortex and hippocampus.

Administration, Inhalation↗
PubMed1990

Routes of chloroform exposure and body burden from showering with chlorinated tap water.

While there is an awareness of the need to quantify inhalation exposure from showers, the potential for dermal exposure to organic contaminants in showers has not been appreciated or explored. To establish routes of environmental exposure from showers, comparisons of the concentration of chloroform in exhaled breath after a normal shower with municipal tap water were made with those after an inhalation-only exposure. The postexposure chloroform breath concentrations ranged from 6.0-21 micrograms/m3 for normal showers and 2.4 to 10 micrograms/m3 for inhalation-only exposure, while the pre-exposure concentrations were all less than the minimum detection limit of 0.86 micrograms/m3. According to an F-test, the difference between the normal shower and the inhalation-only exposures was considered significant at a probability of p = 0.0001. Based on the difference, the mean internal dose due to dermal exposure was found to be approximately equal to that due to the inhalation exposure. The effect of the showering activities on the concentration of chloroform shower air was examined by comparing air concentrations during a normal shower with the air concentrations obtained when the shower was unoccupied. The F-test showed that there is no significant difference between the two sets of data.

Air Pollutants↗
PubMed2002

Benzene metabolism by the isolated perfused lung.

Benzene is an occupational hazard and environmental toxicant whose toxic effects are dependent on its metabolism by cytochrome P-450. Most physiologically based pharmacokinetic models assume that benzene is metabolized only in the liver. They may not be completely accurate in predicting metabolism, especially following inhalation exposure, if metabolism by the lung is important. In the current study, the metabolizing capability of the lung was examined in an in vivo simulation using the isolated perfused lung. Lungs from the rabbit, rat, and mouse were used to mimic benzene metabolism following exposure via the pulmonary vasculature. With the isolated perfused mouse lung, three concentrations (55 microM, 120 microM, and 200 microM) were used to evaluate concentration dependence. To evaluate the ability of the lung to metabolize inhaled benzene, the isolated perfused mouse lung was exposed to benzene (approximately 175 ppm) via the trachea. Benzene was metabolized in all species, with phenol being the major metabolite. Phenylsulfate was also detected in perfusate from rabbits and mice but at much lower levels. Benzene metabolism was concentration dependent in mice. The ability of the lung to metabolize benzene during inhalation exposure was demonstrated in the isolated perfused mouse lung. These results demonstrate that the lung can metabolize benzene in an in vivo simulation when exposed via the pulmonary vasculature or via inhalation.

Air Pollutants, Occupational↗
PubMed1987

The clearance of manganese chloride in the primate.

Two macaque monkeys inhaled trace amounts of 54MnCl2 for 30 min. Subsequently the chest, head, and fecal radioactivity were monitored for over a year. The chest data curve required a sum of three exponential terms, with half-times ranging from 0.2 to 187 days, to attain a satisfactory fit. Head levels peaked 40 days after acute inhalation exposure and remained elevated for over a year. The excretion of manganese through the feces was best described by a sum of two exponentials. One had a half-time of less than 1 day and the second had a half-time of 50 to 60 days. A third macaque received a 6-week continuous exposure to 54Mn through a subcutaneous osmotic pump. With this route, manganese clearance from the head occurred at a faster rate than after acute inhalation exposure. Fecal elimination following continuous subcutaneous exposure resembled that following acute inhalation. Kinetic analyses suggested that the long half-times of manganese in the head following inhalation reflected both slow disappearance from the head and replenishment from other depots.

Animals↗
PubMed2004

The influence of single or repeated low-level sarin exposure on immune functions of inbred BALB/c mice.

To study the influence of single or repeated low-level sarin inhalation exposure on immune functions, inbred BALB/c mice were exposed to low clinically asymptomatic concentrations of sarin for 60 min. in the inhalation chamber. The evaluation of immune functions was carried out using phenotyping of CD3 (T-lymphocytes), CD4 (helper T-lymphocytes), CD8 (cytotoxic T-lymphocytes) and CD19 (B-lymphocytes) in the lungs, blood and spleen, lymphoproliferation of spleen cells stimulated in vitro by various mitogens (concanavalin A, lipopolysaccharides), phagocyte activity of peritoneal and alveolar macrophages, production of N-oxides by peritoneal macrophages and the measurement of the natural killer cell activity at one week after sarin exposure. The results were compared to the values obtained from control mice exposed to pure air instead of sarin. The results indicate that an asymptomatic dose of sarin is able to alter the reaction of the immune system at one week after exposure to sarin. While the number of CD3 cells in lung was significantly decreased, a slight increase in CD19 cells was observed especially in the lungs after a single sarin inhalation exposure. Lymphoproliferation was significantly decreased regardless of the mitogen and sarin concentration used and the number of low-level sarin exposures. The ability of peritoneal and alveolar macrophages to phagocyte the microbes was also decreased regardless of the number of low-level sarin exposures. The production of N-oxides by peritoneal macrophages was decreased following a single low-level sarin exposure but increased following repeated low-level sarin inhalation exposure. Nevertheless, the changes in the production of N-oxides that reflects a bactericidal activity of peritoneal macrophages was not significant. The natural killer cell activity was significantly higher in the case of inhalation exposure of mice to low concentration of sarin regardless of the number of exposures. Thus, not only organophosphorous insecticides but also nerve agents such as sarin are able to alter immune functions following a single inhalation exposure even at a dose that does not cause clinically manifested intoxication. Generally, the repeated exposure to low concentrations of sarin does not increase the alteration of immune functions compared to the single low-level sarin exposure with the exception of phagocyte activity of alveolar macrophages and natural killer cell activity.

Administration, Inhalation↗
PubMed2002

Lung expression of cytochrome P450 1A1 as a possible biomarker of exposure to diesel exhaust particles.

Polycyclic aromatic hydrocarbons (PAH) and reactive oxygen species (ROS) derived from diesel exhaust particles (DEP) are implicated in the pathophysiology of respiratory diseases. Cytochrome P450 (Cyp) 1A1 can be induced by several kinds of PAH and produce ROS. We determined whether acute inhalation exposure to DEP induced the expression of Cyp 1A1 in murine lung. Intratracheal instillation of DEP dose-dependently increased the lung expression of Cyp 1A1 at the levels of both mRNA and protein, whereas DEP decreased expression in the lung of aryl hydrocarbon receptors in a dose-dependent manner. In contrast, charcoal particles as the control did not affect the expression of these molecules. These results suggest that the lung expression of Cyp 1A1 can be a biomarker of acute inhalation exposure to DEP and may be implicated in an accelerated production of ROS and the subsequent aggravation of lung injury.

Animals↗
PubMed1996

Assessment of 1,3-butadiene mutagenicity in the bone marrow of B6C3F1 lacI transgenic mice (Big Blue): a review of mutational spectrum and lacI mutant frequency after a 5-day 625 ppm 1,3-butadiene exposure.

1,3-Butadiene (BD) is a carcinogen that is bioactivated to at least two genotoxic metabolites. In the present article, we review briefly our previous studies on the in vivo mutagenicity and mutational spectra of BD in bone marrow and extend these studies to examine the effect of exposure time (5-days vs. 4-week exposure to 625 ppm BD used in previous studies) on the lacI mutant frequency in the bone marrow. Inhalation exposure to BD at 625 ppm and 1,250 ppm mutagenic in vivo, inducing an increase in the transgene mutant and mutation frequency in the bone marrow. Analysis of the mutational spectrum in BD-exposed and air control mice demonstrated that BD exposure induced an increased frequency of mutations at A:T base pairs. There was no difference in the lacI mutant frequency determined in the bone marrow between a short-term exposure to BD (5 days) and a longer-term exposure (4 weeks). These data taken together demonstrate that inhalation exposure to BD induces in vivo somatic cell mutation.

Administration, Inhalation↗
PubMed2006

Efficient activation of aflatoxin B1 by cytochrome P450 2A13, an enzyme predominantly expressed in human respiratory tract.

The worldwide human exposure to aflatoxin B1 (AFB1), particularly in developing countries, remains to be a serious public health concern. Although AFB1 is best known as a hepatocarcinogen, epidemiological studies have shown a positive association between human lung cancer occurrence and inhalation exposure to AFB1. Cytochrome P450 (CYP)-catalyzed metabolic activation is required for AFB1 to exert its carcinogenicity. Previous studies have identified CYP1A2 and CYP3A4 as the major enzymes for AFB1 activation in human liver. However, the key CYP enzymes in human lung that can efficiently activate AFB1 in situ are unknown. In the present study, we demonstrate that CYP2A13, an enzyme predominantly expressed in human respiratory tract, has a significant activity in metabolizing AFB1 to its carcinogenic/toxic AFB1-8,9-epoxide and AFM1-8,9-epoxide at both low (15 microM) and high (150 microM) substrate concentrations. Under the same conditions, there was no detectable AFB1 epoxide formation by CYP2A6, which was also reported to be involved in the metabolic activation of AFB1. Consistent with the activity data, there was an approximately 800-fold difference in LC50 values of AFB1 (48-hr treatment) between Chinese hamster ovary (CHO) cells expressing CYP2A13 and CYP2A6 (50 nM versus 39 microM). We further demonstrate that amino acid residues Ala117 and His372 in CYP2A13 protein are important for AFB1 epoxidation and its related cytotoxicity. Our results suggest that CYP2A13-catalyzed metabolic activation in situ may play a critical role in human lung carcinogenesis related to inhalation exposure to AFB1.

Aflatoxin B1↗
PubMed2003

Occupational methaemoglobinaemia. Mechanisms of production, features, diagnosis and management including the use of methylene blue.

Methaemoglobin is formed by oxidation of ferrous (FeII) haem to the ferric (FeIII) state and the mechanisms by which this occurs are complex. Most cases are due to one of three processes. Firstly, direct oxidation of ferrohaemoglobin, which involves the transfer of electrons from ferrous haem to the oxidising compound. This mechanism proceeds most readily in the absence of oxygen. Secondly, indirect oxidation, a process of co-oxidation which requires haemoglobin-bound oxygen and is involved, for example, in nitrite-induced methaemoglobinaemia. Thirdly, biotransformation of a chemical to an active intermediate that initiates methaemoglobin formation by a variety of mechanisms. This is the means by which most aromatic compounds, such as amino- and nitro-derivatives of benzene, produce methaemoglobin. Methaemoglobinaemia is an uncommon occupational occurrence. Aromatic compounds are responsible for most cases, their lipophilic nature and volatility facilitating absorption during dermal and inhalational exposure, the principal routes implicated in the workplace. Methaemoglobinaemia presents clinically with symptoms and signs of tissue hypoxia. Concentrations around 80% are life-threatening. Features of toxicity may develop over hours or even days when exposure, whether by inhalation or repeated skin contact, is to relatively low concentrations of inducing chemical(s). Not all features observed in patients with methaemoglobinaemia are due to methaemoglobin formation. For example, the intravascular haemolysis caused by oxidising chemicals such as chlorates poses more risk to life than the methaemoglobinaemia that such chemicals induce. If an occupational history is taken, the diagnosis of methaemoglobinaemia should be relatively straightforward. In addition, two clinical observations may help: firstly, the victim is often less unwell than one would expect from the severity of 'cyanosis' and, secondly, the 'cyanosis' is unresponsive to oxygen therapy. Pulse oximetry is unreliable in the presence of methaemoglobinaemia. Arterial blood gas analysis is mandatory in severe poisoning and reveals normal partial pressures of oxygen (pO2) and carbon dioxide (pCO2,), a normal 'calculated' haemoglobin oxygen saturation, an increased methaemoglobin concentration and possibly a metabolic acidosis. Following decontamination, high-flow oxygen should be given to maximise oxygen carriage by remaining ferrous haem. No controlled trial of the efficacy of methylene blue has been performed but clinical experience suggests that methylene blue can increase the rate of methaemoglobin conversion to haemoglobin some 6-fold. Patients with features and/or methaemoglobin concentrations of 30-50%, should be administered methylene blue 1-2 mg/kg/bodyweight intravenously (the dose depending on the severity of the features), whereas those with methaemoglobin concentrations exceeding 50% should be given methylene blue 2 mg/kg intravenously. Symptomatic improvement usually occurs within 30 minutes and a second dose of methylene blue will be required in only very severe cases or if there is evidence of ongoing methaemoglobin formation. Methylene blue is less effective or ineffective in the presence of glucose-6-phosphate dehydrogenase deficiency since its antidotal action is dependent on nicotinamide-adenine dinucleotide phosphate (NADP+). In addition, methylene blue is most effective in intact erythrocytes; efficacy is reduced in the presence of haemolysis. Moreover, in the presence of haemolysis, high dose methylene blue (20-30 mg/kg) can itself initiate methaemoglobin formation. Supplemental antioxidants such as ascorbic acid (vitamin C), N-acetylcysteine and tocopherol (vitamin E) have been used as adjuvants or alternatives to methylene blue with no confirmed benefit. Exchange transfusion may have a role in the management of severe haemolysis or in G-6-P-D deficiency associated with life-threatening methaemoglobinaemia where methylene blue is relatively contraindicated.

Enzyme Inhibitors↗
PubMed1994

T cell functions are impaired by inhaled isobutyl nitrite through a T-independent mechanism.

Isobutyl nitrite is representative of a group of inhalants abused by male homosexuals and adolescents. Inhalation exposure of mice to isobutyl nitrite at 900 ppm for 45 min per day for 14 days caused serious deficits in T cell-mediated immune responses. Cytotoxic T lymphocyte (CTL) activity was reduced by 36% following the exposure. T cell proliferative responses to mitogenic and allogeneic stimulation were reduced by 37% and 51%, respectively. The exposure did not directly alter the ability of cells to synthesize or respond to IL-2. Accessory cell function in facilitating T cell activation was inhibited by about 50% following exposure to the inhalant.

Administration, Inhalation↗
PubMed2002

Cytotoxicity by nitrite inhalants is not related to peroxynitrite formation.

Nitrite inhalant abuse has been correlated with HIV and Kaposi's sarcoma. Mouse models of inhalant exposure show immunosuppression and loss of immune cells. In the present study, isobutyl nitrite caused a dose-dependent loss of viability of a macrophage cell line. In the absence of cells, isobutyl nitrite reacted with hydrogen peroxide to form peroxynitrite. However, assays of mitochondrial respiration and nitration that detect peroxynitrite indicated that very little was present in cell cultures following exposure to the inhalants. Isobutyl, isoamyl, and butyl nitrites inhibited mitochondrial respiration, but only at high concentrations. Similarly, the nitrating activity of isobutyl nitrite occurred only at high concentrations and was not affected by the presence of hydrogen peroxide. Western blots showed that the inhalant did not increase nitrotyrosine formation in RAW cells or in peritoneal exudate macrophages (PEM) from exposed mice. Thus, the toxicity induced by isobutyl nitrite was probably not due to peroxynitrite formation.

Administration, Inhalation↗
PubMed1991

Percutaneous absorption of 2-butoxyethanol vapour in human subjects.

Four male volunteers were exposed at rest for two periods of two hours, separated by a one hour exposure free interval, to 50 ppm 2-butoxyethanol (BE) vapour generated in an exposure chamber. During the first two hour period the men were exposed by mouth only via a respiratory valve connected by tubes to the exposure chamber. During the second exposure period the men were exposed by skin only while sitting inside the exposure chamber, naked except for shorts, and wearing a respiratory protection mask supplied with compressed air. Capillary blood samples were collected at regular intervals and analysed for BE by a gas chromatographic method. Two experiments separated by at least two weeks were carried out with each volunteer, one at "normal" (23 degrees C, 29% relative humidity) and one at raised (33 degrees C, 71% relative humidity) air temperature and humidity in the chamber. The average concentration in blood and the calculated rate of uptake of BE were about three to four times higher during dermal exposure than during inhalation exposure. These experiments suggest that dermal uptake of BE accounts for about 75% (45-85% in individual experiments) of the total uptake during whole body exposure to BE vapour. Thus it appears that the use of a respiratory protection mask will not protect efficiently against exposure to BE vapours. A tendency towards increased percutaneous absorption rate was seen in the raised temperature and humidity condition.

Adult↗
PubMed1993

Occupational and environmental exposures reported to poison centers.

This analysis of 25,368 occupational and 7,565 environmental exposure cases characterizes the occupational and environmental exposures reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System. Compared with other poisonings, occupational and environmental exposures were predominantly inhalation exposures rather than ingestions, were more often subacute or chronic, and demonstrated greater morbidity, mortality, and increased use of health care resources. As regional poison centers evolve to fill a critical information void in the management and assessment of environmental and occupational exposures, the American Association of Poison Control Centers Toxic Exposure Surveillance System provides an important, untapped passive surveillance mechanism.

Air Pollutants↗
PubMed1978

Percutaneous absorption of solvent vapors in man.

It is known from industrial experience and experimental studies that percutaneous absorption of concentrated liquid solvents may be considerable and even hazardous if large enough areas of skin are exposed for long periods of time. Percutaneous penetration of xylene, styrene, toluene, 1,1,1-trichloroethane and tetrachloroethylene vapors at ambient air concentrations of 600 ppm for 3.5 h was studied in a dynamic exposure chamber with a restricted number of human volunteers. Although the small number of exposed persons precluded conclusive quantitation of absorption and valid intercompound comparisons, aromatic solvents and tetrachloroethylene appear to penetrate skin much more readily than 1,1,1-trichloroethane. Skin penetrating properties of solvents seem, under the circumstances, to be associated primarily with lipid solubility. It was approximated that percutaneous exposure (total body surface) to 600 ppm of xylene vapor for 3.5 h corresponded to an equally long inhalation exposure of less than 10 ppm. Similar percutaneous exposure to 1,1,1,-trichloroethane corresponded to an inhalation exposure of only 0.6 ppm. Disease-affected skin may display altered permeability characteristics, and one volunteer with atopic dermatitis exhibited a more than three times larger absorption of xylene vapor when compared to subjects with normal skin. It may be concluded that in the work environment percutaneous absorption of solvent vapors from the surrounding air through undamaged skin is likely to be insignificant.

Adult↗
PubMedDate not supplied

[Occupational exposure to inhalation anesthetics: 10 years of measurements at hospitals in Puglia].

The Authors provide the data gathered from measurements of nitrous oxide in the operating room of Puglia during the period between 1993 and 2003. They prove significant reductions of pollution according with time and they verify lower pollution levels in the operating rooms of private hospitals with respect to public facilities. The importance of the maintenance of gas distribution and evacuation systems is shown and a method of environmental and biological monitoring is provided. Finally, the Authors prove the utility of the graphic representation of the measurements, conduced utilising dedicated instrumentation.

Air Pollution, Indoor↗