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Occupational exposure to inhalational anesthetics during cardiac surgery on cardiopulmonary bypass.

BACKGROUND: Eventual hazards from occupational exposure of operating room personnel to inhalational anesthetic agents cannot yet be definitively excluded. We determined if occupational exposure of operating room personnel to waste anesthetic gases during cardiopulmonary bypass (CPB) complies with the established governmental limits. METHODS: Ten adults underwent inhalational anesthesia for coronary artery bypass grafting with nitrous oxide and either sevoflurane (n = 5) or desflurane (n = 5). The administration of inhalational anesthetic agents was stopped before initiation of CPB. Gas samples were obtained before and during CPB every 90 seconds from the breathing zones of anesthesiologist (A), surgeon (S), and perfusionist (P). Time-weighted averages (TWA) over the time of exposure were calculated. RESULTS: The surgeon's exposure to nitrous oxide was 9.3 +/- 1.9 parts per million (ppm) before and 3.0 +/- 1.4 ppm during CPB (A: 6.7 +/- 1.1 ppm and 0.5 +/- 0.1 ppm; P: 3.7 +/- 1.4 ppm during CPB). Occupational exposure to desflurane was 0.21 +/- 0.10 ppm before and 0.62 +/- 0.28 ppm during CPB for the surgeon (A: 0.02 +/- 0.01 ppm and 0.02 +/- 0.003 ppm; P: 0.82 +/- 0.26 ppm during CPB), thereby exceeding the given limit of 0.5 ppm. Exposure levels of sevoflurane were below the 0.5 ppm limit at all times, as were nitrous oxide levels (threshold limit: 25 ppm). CONCLUSIONS: Although occupational exposure to inhalational anesthetic agents was low at most times during the study and none of the operating room staff complained about subjective or objective impairment or discomfort, all measures must be taken to further minimize occupational exposure, including sufficient air conditioning and routine use of waste gas scavenging systems on CPB equipment.

Adult↗

Inhalable dust exposures, tasks, and use of ventilation in small woodworking shops: a pilot study.

Measures of workers' inhalable dust exposures, tasks, and ventilation use were made in five small woodworking shops prior to the start of an intervention effectiveness study aimed at lowering personal wood dust exposures. The data were used to (1) design a sampling protocol for an intervention success measure, (2) identify targets for intervention among the tasks and activities responsible for high dust levels, and (3) develop shop-level measures as tools for tailoring intervention activities. Geometric mean dust concentrations ranged from 1.6 to 9.9 mg/m3 in the five shops, with the highest levels occurring in a cabinet shop. All shops had centralized dust collection systems and workers generally used dust control on stationary tools (60-100% of the time) when it was available. Sanding with both stationary and handheld powered tools, cleaning with methods that can disperse dust (e.g., brushes, compressed air), and miscellaneous tasks were all responsible for significant personal exposures. The positive association between miscellaneous tasks and exposures probably reflects the high background levels generated by nearby processes. Sanding with both stationary tools and handheld powered tools represents the most significant influence on personal exposures in small woodworking shops. The authors conclude that pilot studies are useful tools for designing occupational health and safety intervention effectiveness studies.

Dust↗

Analysis of rat testicular protein expression following 91-day exposure to JP-8 jet fuel vapor.

We analyzed protein expression in preparations from whole testis in adult male Sprague-Dawley rats exposed for 6 h/d for 91 consecutive days to jet propulsion fuel-8 (JP-8) in the vapor phase (0, 250, 500, or 1000 mg/m(3) +/- 10%), simulating a range of possible human occupational exposures. Whole body inhalation exposures were carefully controlled to eliminate aerosol phase, and subjects were sacrificed within 48 h postexposure. Organ fractions were solubilized and separated via large-scale, high resolution two-dimensional electrophoresis, and gel patterns scanned, digitized and processed for statistical analysis. Seventy-six different testis proteins were significantly increased or decreased in abundance in vapor-exposed groups, compared to controls, and dose-response profiles were often nonlinear. A number of the proteins were identified by peptide mass fingerprinting and related to histopathological or physiological deficits shown in previously published studies to occur with repeated exposure to hydrocarbon fuels or solvents. These results demonstrate a significant effect of JP-8 exposure on protein expression, particularly in protein expression in the rodent testis, and suggest that a 91 d exposure to jet fuel vapor induces changes of equal or greater magnitude to those reported previously for shorter duration JP-8 aerosol exposures.

Administration, Inhalation↗

Morbidity following acute irritant inhalation in a population-based study.

STUDY OBJECTIVE: To estimate the incidence of and risk factors for morbidity due to inhalation of respiratory irritants. DESIGN: Six-month case series of inhalational exposures reported to a poison control center with follow-up, structured interviews of subjects. SETTING: A regional poison control center providing 24-hour telephone consultation to health professionals and the public. PATIENTS: Consecutive sample of 683 inhalation cases, with interviews of 323 subjects. MEASUREMENTS AND MAIN RESULTS: Moderate to severe irritants accounted for 160 (50%) of the inhalational exposures in interviewed subjects. Persistent symptoms lasting 14 days or longer were reported by only 20 (6%) of the subjects. Irritant exposure was a statistically significant risk factor for acute respiratory symptoms (relative risk [RR] = 1.7; 95% confidence interval [Cl], 1.4 to 2.1) but was unrelated to persistent symptoms. Preexisting lung conditions (RR = 2.4; 95% Cl, 1.4 to 4.2) and cigarette smoking (RR = 1.7; 95% Cl, 1.3 to 2.2) were both statistically significant risk factors for persistent symptoms. CONCLUSIONS: Symptomatic inhalational exposures due to irritants are frequent in reports from poison control centers. Residual morbidity was uncommon and did not appear to be statistically related to the degree of irritant exposure. Host-related factors may be better predictors of ongoing morbidity after inhalational exposure.

Age Factors↗

Occupational exposure to inhalable and total aerosol in the primary nickel production industry.

OBJECTIVES: This paper describes a study that was carried out in the primary nickel production industry to investigate the levels of personal exposure to aerosols containing nickel and the impact on exposure assessment of introducing new personal sampling techniques with performance consistent with the latest particle size-selective criteria. METHODS: Experiments were carried out at workplaces in mining, milling, smelting, and refining works to investigate the effect of changing from the current method of total aerosol (with the widely used 37 mm filter holder) to the new method of measuring inhalable aerosol (with the Institute of Occupational Medicine (IOM) inhalable aerosol sampler). RESULTS: The results show that inhalable aerosol exposure concentrations--for both overall aerosol and for total nickel--were consistently and significantly higher than the corresponding total aerosol concentrations. Weighted least squares linear regression yielded IOM/37 mm factors ranging from about 1.2 to 4.0. The exposure data for each company process were found to be log-normally distributed. CONCLUSIONS: The results suggest the possibility of generating a single pragmatic factor for each company process for converting current total aerosol exposures to new exposures based on the inhalability concept contained in the latest particle size-selective criteria for aerosol exposure assessment. Such data may be important in determining new occupational exposure limits for nickel.

Aerosols↗

Respiratory aflatoxicosis: suppression of pulmonary and systemic host defenses in rats and mice.

Dietary aflatoxin B1 (AFB1) exposure impairs innate and acquired host defenses resulting in increased susceptibility to infections in domesticated animals. Experimental studies have confirmed this observation by demonstrating the immunosuppressive effects of AFB1 ingestion. In addition to being present in dietary components, AFB1 is also found in significant amounts in respirable particles of grain dust. To determine the effect of respiratory tract exposure to AFB1 on host defenses, rats and mice were exposed either by aerosol inhalation or intratracheal instillation to AFB1. Nose-only inhalation exposure of rats to AFB1 aerosols suppressed alveolar macrophage (AM) phagocytosis at an estimated dose of 16.8 micrograms/kg with the effect persisting for approximately 2 weeks. To determine whether another mode of respiratory tract exposure, intratracheal instillation, reflected inhalation exposure, animals were treated with increasing concentrations of AFB1 which also suppressed AM phagocytosis in a dose-related manner albeit at doses at least an order of magnitude more than that obtained by aerosol inhalation. Intratracheal administration of AFB1 also suppressed the release of tumor necrosis factor-alpha from AMs and impaired systemic innate and acquired immune defenses as shown, respectively, by suppression of peritoneal macrophage phagocytosis and the primary splenic antibody response. These findings demonstrate that experimental respiratory tract exposure to AFB1 suppresses pulmonary and systemic host defenses and indicates that inhalation exposure to AFB1 is an occupational hazard where exposure to AFB1-laden dust is common.

Administration, Inhalation↗

Circulating factors that modify lung cell DNA synthesis following exposure to inhaled oxidants. I. Effect of serum and lavage on lung fibroblasts following exposure of adult rats to 1 ppm ozone.

Adult rats were exposed to 1 ppm (1.96 mg/m3) ozone or air for 2 wk. Animals were sacrificed at 3, 5, 7, or 14 d after the onset of exposure, and samples of plasma and lung lavage were obtained. Heat-inactivated plasma, from animals exposed to ozone for 7 or 14 d, significantly increased DNA synthesis by lung fibroblasts compared with plasma from air-exposed animals. Fractionation of plasma and lavage samples indicated that the factor responsible had an isoelectric point of 6.45-6.75 and a molecular weight of 32 +/- 2 kDa. This factor has a dose-dependent effect on lung fibroblast DNA synthesis in culture, but no significant effect on cultured pneumocyte DNA synthesis. The factor is detectable within 72 h of exposure, and may hold some promise as a marker of early oxidant lung injury.

Animals↗

Formaldehyde exposure enhances inhalative allergic sensitization in the guinea pig.

Formaldehyde (FA), a common indoor air pollutant, has been associated with increased prevalence rates of asthmatic symptoms among exposed individuals in epidemiologic surveys. We studied the influence of FA exposure on inhalative allergic sensitization in the guinea pig. Three groups of guinea pigs (n = 12 each) were exposed to clean air or two different FA concentrations (0.13 and 0.25 ppm) over 5 consecutive days. Exposure was followed by inhalation of 0.5% ovalbumin (OA) as sensitizing allergen. Three weeks later, specific bronchial provocation with OA was performed with body plethysmographic measurement of compressed air (CA). Furthermore, specific anti-OA-IgGl (reaginic) antibodies were determined in serum. In a further six animals, the respiratory tract was examined histologically for signs of inflammation directly after the end of FA or clean air exposure. In the group exposed to 0.25 ppm FA, 10/12 animals were found to be sensitized to OA (positive reaction on specific provocation) vs. 3/12 animals in the control group (P < 0.01). Furthermore, CA measurements of specific bronchial provocation and serum anti-OA-antibodies were significantly higher in the 0.25 ppm FA group than in controls (CA 0.35 vs. 0.09 ml median, P < 0.01; anti-OA-IgGl 13 vs. < 10 EU median, P < 0.05), indicating enhanced sensitization. In the group exposed to 0.13 ppm FA, no significant difference was found compared to the control group. There was no sign of inflammation of the lower airways in FA-exposed guinea pigs other than mucosal edema, which was discovered by morphometry. We conclude that short-term exposure to a low concentration of FA (0.25 ppm) can significantly enhance sensitization to inhaled allergens in the guinea pig.

Allergens↗

Biological monitoring of N, N-dimethylformamide. Reference value for N-methylcarbamoyl adduct at the N-terminal valine of globin as a biomarker of chronic occupational exposure.

OBJECTIVES: The recently identified metabolic product of the industrial solvent N, N-dimethylformamide (DMF), the N-methylcarbamoyl adduct at the N-terminal valine of globin, can be determined after chemical conversion to 3-methyl-5-isopropylhydantoin (MVH). Due to prolonged persistence of the adduct in human erythrocytes (lifetime: 4 months), MVH is a suitable biomarker of integrated exposure to DMF over a period of several months. Here we propose a reference value for MVH, used for biological monitoring of chronic occupational exposure to DMF. METHODS: The reference value for MVH was set equal to its steady-state level in a simulated repeated inhalation exposure to DMF (8 h/day, 5 days/week, >or=20 weeks) at a concentration corresponding to the occupational exposure limits MAK and TLV. The initial data on the toxicokinetic behavior of MVH were obtained after single percutaneous and inhalation exposures to DMF in volunteers. MVH was determined by gas chromatography-mass spectrometry according to Mráz et al. RESULTS: The steady-state level of MVH, attained after repeated inhalation exposure to DMF, 30 mg/m(3), 8 h/day, 5 days/week, >or=20 weeks, was assessed to be approximately 135 nmol MVH/g globin. CONCLUSIONS: We recommend the value of 135 nmol MVH/g globin to be used as a new reference value for biomonitoring of integrated exposure to DMF over a long period. The relationship between the MVH level in globin and the intensity of the exposure to DMF should be further tested in the field studies.

Biomarkers↗

Loss of postural reflexes in long-term occupational solvent exposure.

Inhalation of organic solvents has long been known to damage various nervous systems, including cerebellum, brainstem, and pyramidal tract. However, little is known about the damage of the dopaminergic system. We report two patients with occupational long-term solvent exposure who developed postural instability without other features of parkinsonism. The concentration of HVA in CSF was decreased and the retropulsion was dramatically improved after the administration of levodopa. These findings indicate that the nigrostriatal dopaminergic neurons were disturbed by chronic solvent exposure, resulting in the loss of postural reflexes.

Adult↗

In vivo metabolism and kinetics of ethylene glycol monobutyl ether and its metabolites, 2-butoxyacetaldehyde and 2-butoxyacetic acid, as measured in blood, liver and forestomach of mice.

1. Ethylene glycol monobutyl ether (EGBE) causes forestomach hyperplasia and neoplasia in mice when administered chronically by inhalation. 2. The study was initiated to test the physiologically based pharmacokinetic (PBPK) model prediction that 2-butoxyacetaldehyde (BAL), a transient, labile intermediate in the oxidation of EGBE to butoxyacetic acid (BAA), is unlikely to achieve concentrations sufficient to cause DNA damage in target tissues. 3. Male and female B6C3F1 mice were administered a high oral dose of EGBE (600mgkg(-1)), and tissues were collected at 5, 15, 45 and 90min following the dose. The tissues were processed for determination of EGBE, BAL and BAA by gas chromatography-mass spectrometry. 4. BAL was detected at low concentrations in all tissues sampled and at all time points following EGBE administration (about 0.3-33 microM). BAL concentrations were highest in the initial samples (5 min) in all tissues and declined from that point. 5. BAL concentrations in liver and forestomach tissues corresponded to the peak concentrations predicted by an already published PBPK model, and are higher than BAL concentrations that could be achieved by inhalation exposure to EGBE. 6. Mouse inhalation exposure to EGBE is therefore unlikely to generate BAL concentrations in tissues sufficient to initiate a carcinogenic response.

Acetaldehyde↗

Exposures to inhalable and "total" oil mist aerosol by metal machining shop workers.

Several recent studies have compared worker personal aerosol exposures as measured by the current method with those obtained by a new approach based on collecting the inhalable fraction, intended to represent all the particles that are capable of entering through the nose and/or mouth during breathing. The present study investigated this relationship for a metal machining facility where aerosols were generated from severely refined, nonaqueous ("straight") cutting oils used during the lathe working of metal rod stock. Workers (n = 23) wore two personal aerosol samplers simulataneously, one of the 37-mm type (for "total" aerosol exposure, E37) and the other of the Institute of Occupational Medicine (IOM) type (for inhalable aerosol exposure, EIOM). The data were analyzed by weighted least squares linear regression to determine the coefficient S in the relation EIOM = S.E37. It was found that S = 2.96 +/- 0.60. This ratio-in which exposure to inhalable aerosol was greater than to "total" aerosol-is consistent with previous observations in other industries. The relative coarsenss of the oil mist aerosol, as estimated by cascade impactor measurements, probably explains the difference between the sampling methods. The collection of large "splash" droplets, may also contribute. Future occupational aerosol standards for metalworking fluids will be based on the new, health-related criteria, and exposures will be assessed on the basis of the inhalable fraction. Results of studies like that described here will enable assessment of the impact on future workplace aerosol exposure assessments of introducing new standards.

Aerosols↗

Tolerance to the miotic effect of sarin vapor in rats after multiple low-level exposures.

Inhibition of acetylcholinesterase (AChE) by the organophosphorous compound sarin (GB) results in the accumulation of acetylcholine and excessive cholinergic stimulation. There are few data in the literature regarding the effects of multiple low-level exposures to GB and other organophosphorous compounds via relevant routes of exposure. Therefore, the present study was undertaken, and is the first, to investigate the effect of low-level repeated whole-body inhalation exposures to GB vapor on pupil size and cholinesterase activity in the eyes and blood. Male Sprague-Dawley rats were exposed to 4.0 mg/m3 of GB vapor for 1 h on each of 3 consecutive days. Pupil size and cholinesterase activities were determined at various points throughout the exposure sequence. The results demonstrate that multiple inhalation exposures to GB vapor produce a decrease in the miotic potency of GB in rats. This tolerance developed at a dose of GB that produced no overt signs of intoxication other than miosis. AChE and butyrylcholinesterase activity did not increase throughout the exposure sequence, suggesting that the tolerance cannot be attributed to a reduced inhibitory effect of GB. A decrease in the amount of GB present in the eye occurred after the third exposure. However, this change is insufficient to explain the tolerance, as there was no corresponding increase in AChE activity. Thus, the mechanism mediating the miotic tolerance observed after multiple inhalation exposures to the nerve agent GB remains uncertain, although several possibilities can be excluded based on the results of the present study.

Acetylcholinesterase↗

Trends in levels of inhalable dust exposure, exceedance and overexposure in the European carbon black manufacturing industry.

In an attempt to investigate the relationship between exposure to carbon black and respiratory morbidity, a study of the complete carbon black manufacturing industry in Western Europe was commissioned. As part of this study, a large number of personal inhalable (n=8015) dust exposure measurements was taken during three phases of data collection between 1987 and 1995. Repeated measurements on the same worker were taken in the last two phases, which enabled the estimation of the within- and between-worker components of variance. Simultaneously, the fixed effects of phase and factory were estimated using mixed-effects analysis of variance. The results show that the personal inhalable dust exposure has reduced significantly since the first phase of the study. In addition, the interaction term between phase and factory was significant in most job categories, confirming that the reduction of exposure was not equal across all factories. When all factories were considered together, the probability that the mean exposure of a randomly selected worker (overexposure) or the probability that the exposure on a randomly selected day for a randomly selected worker (exceedance) was higher than 3.5mg m(-3), was 10% or less for all job categories in the last phase. However, when the factories were considered separately, it appeared that the probability of overexposure or exceedance was in excess of 10% for the job categories 'Fitter/Welder', 'Warehouseman' and 'Site crew' for a number of factories. Therefore, even though exposure levels of inhalable dust have dropped considerably across the whole carbon black manufacturing industry in Western Europe, further reductions in exposure levels are required in these areas to make sure that the probability of overexposure and exceedance falls below a level of 10%.

Air Pollutants, Occupational↗

Rat brain DNA transcript profile of halothane and isoflurane exposure.

Inhaled anesthetics produce many effects and bind to a large number of brain proteins, but it is not yet clear if this is accompanied by widespread changes in gene expression of the biological targets. Such changes in expression might implicate functionally important targets from the large pool of binding targets. Both rats and isolated primary cortical neurons were exposed to anesthetics and DNA oligonucleotide microarrays were used to detect and quantify transcriptional changes in neural tissue. Using analysis of variance with multiple testing correction, multiple exposures of rats to 0.8 MAC (minimum alveolar concentration) halothane only produced significant changes in a few metabolic genes. No significant in-vivo gene transcriptional response to 0.8 MAC isoflurane was detected. The use of primary cortical neurons allowed exposure to 3 MAC anesthetics without evidence of toxicity. Isoflurane altered several genes involved with neurotransmitter transport, signaling and cellular structure, whereas halothane produced few detectable changes in these cultured cells. Selected genes were confirmed by quantitative reverse transcription-polymerase chain reaction. Although indicating only a small degree of transcriptional regulation, these data implicate several plausible targets, including synaptic vesicle handling, that might contribute to drug action. In addition, the data show different gene expression profiles for the two inhaled anesthetics, suggesting unique pharmacological targets and mechanisms in each case.

Anesthetics, Inhalation↗

A follow-up study on occupational exposure to inhaled anaesthetics in Eastern European surgeons and circulating nurses.

OBJECTIVE: Although no dose-response relationship exists for the health risks associated with the occupational exposure to inhaled anaesthetics, public health authorities recommend threshold values. The aim of the present study was to assess whether and to what extent these threshold values are exceeded in surgeons and circulating nurses of an Eastern European university hospital, before and after measures had been taken to reduce occupational exposure. METHODS: At nine workplaces, occupational exposure to nitrous oxide and the volatile anaesthetic used (halothane or isoflurane) was measured within the breathing zones of surgeons and circulating nurses by means of photoacoustic infrared spectrometry. The measurements were carried out in 1996 and were repeated in 1997 after the installation of active scavenging devices at five workplaces, and an air-conditioning system at one workplace. RESULTS: Occupational exposure to nitrous oxide and halothane or isoflurane was lower in 1997 compared with that of 1996. In 1996, 89% of the nitrous oxide values were above the European threshold value of 100 ppm, whereas in 1997 approximately 50% were above this limit. In 1996 the majority of the measurements for the volatile anaesthetics were already below 5 ppm halothane and 10 ppm isoflurane and the number of measurements exceeding these limits was further reduced in 1997. CONCLUSION: The measures taken were effective in reducing waste gas exposure. Nevertheless, further efforts are necessary, especially for nitrous oxide, to reach Western European standards and to minimise possible health risks. These efforts comprise the installation of (active) scavenging devices, air-conditioning systems and new anaesthesia machines at all workplaces, the use of low-flow anaesthesia, the replacement of inhaled anaesthetics by intravenous anaesthetics and an appropriate working technique.

Anesthetics, Inhalation↗

Respiratory sensitization to diphenyl-methane-4,4'-diisocyanate (MDI) in guinea pigs: impact of particle size on induction and elicitation of response.

The impact of particle size of aerosolized polymeric diphenylmethane-4,4'-diisocyanate (MDI) for the induction and elicitation of respiratory sensitization was evaluated. Four groups of 16 female guinea pigs each received either the vehicle, repeated intradermal (id) injections (3 x 0.3% MDI), one high-level inhalation exposure of 15 min to 135 mg MDI/m(3) air using a small aerosol (MMAD approximately 1.7 microm) or large aerosol (MMAD approximately 3.8 microm). Three weeks later, animals were challenged subsequently with two ramped concentrations of MDI aerosol (average concentrations 16 and 49 mg/m(3) air, each for 15 min) and two different particle sizes, i.e., the MMAD was either approximately 1.6 microm or approximately 5.1 microm for the small- and large-size aerosol, respectively. Respiratory sensitization was assessed by two endpoints: the measurement of respiratory rate, and examination of influx of eosinophilic granulocytes into the mucosa and submucosa of the trachea, bronchi, and lung-associated lymph nodes (LALN). The recruitment of eosinophilic granulocytes into bronchial tissues was subdivided as follows: muscularis mucosae, submucosa, and perivascular. From measurements of respiratory rate, it would appear that guinea pigs sensitized by id injections or by inhalation exposure with the large aerosol tended to display a higher responsiveness than naive controls when challenged with the small aerosol. The recruitment of eosinophilic granulocytes in the bronchial tissue was greater in both inhalation induction groups as compared to the vehicle control. It appears that there was a somewhat greater response in animals sensitized by id injections or by inhalation exposure with the large aerosol and challenged with the small aerosol. Topographically, this difference was apparent only at the bronchial perivascular level and lung-associated lymph nodes (LALN), whereas at the submucosal and muscularis mucosae level the impact on particle size tended to be less pronounced. In summary, this study suggests that a brief, high-level inhalation exposure of MDI aerosol caused a sensitization of bronchial tissues in guinea pigs. The higher sensitization potency of the large aerosol may possibly be related to a dosimetric phenomenon because of the greater fraction of deposition of large particles within the upper respiratory tract. Overall, challenge exposures with this type of irritant aerosol appear to evoke more consistent effects when the MMAD is in the range of approximately 2 rather than approximately 5 microm.

Administration, Inhalation↗

Exposure to inhaled isobutyl nitrite reduces T cell blastogenesis and antibody responsiveness.

Isobutyl nitrite is a drug of abuse popular among male homosexuals and among adolescents. In order to approximate the nitrite exposures of inhalant abusers, mice were treated with 900 ppm isobutyl nitrite in an inhalation chamber for 45 min per day for 14 days. After 14 consecutive days of exposure to isobutyl nitrite, mice weighed an average of 4% less than mice exposed to air. The spleens of nitrite-exposed mice weighed 15% less and had 24% fewer cells per spleen than those of controls. Adjusted for equal cell numbers, T cell mitogenic and allogeneic proliferative responses were significantly reduced by 33 and 47%, respectively. The frequency of T-dependent plaque-forming cells (PFC) was inhibited by 63% and the total number of PFC per spleen was reduced by 72% in nitrite-exposed mice. In contrast, B cell proliferative responses to LPS were unaltered, suggesting that the toxicity of isobutyl nitrite did not affect all lymphoid cells equally. The data suggest that habitual inhalation of isobutyl nitrite could impair immune competence and that toxicity appeared to be directed toward T cell functions.

Administration, Inhalation↗