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PubMed1997

Application of tryptamine as a derivatizing agent for the determination of airborne isocyanates. Part 7. Selection of impinger solvents and the evaluation against dimethyl sulfoxide used in US NIOSH Regulatory Method 5522.

The application of tryptamine to derivatize airborne isocyanates has been evaluated and adopted by the National Institute for Occupational Safety and Health (NIOSH) as the latest isocyanates regulatory method (Method 5522) in the USA. Method 5522 uses dimethyl sulfoxide (DMSO) as the impinger solvent in which tryptamine is dissolved to sample isocyanates for analysis. Since DMSO is both extremely hygroscopic and corrosive, it is not a satisfactory solvent for impinger air sampling of isocyanates. The high boiling and freezing points also present some distinct drawbacks. In a search for a suitable impinger solvent, the efficiencies of various solvents, which all were potentially more suitable for sampling isocyanates viz., N,N'-dimethylformamide, butyl acetate, isobutyl acetate, sec-butyl acetate, tert-butyl acetate and octane, were investigated. Simulated air sampling was conducted on two commonly used isocyanates in industry, hexamethylene diisocyanate (HDI) and toluene diisocyanate (TDI), which were vaporized and sampled into impingers containing dissolved tryptamine. Butyl acetate and octane were found to be most suitable for using as impinger solvents. Recoveries of isocyanates at two concentration levels of HDI and TDI were 93.4-108% in comparison with those of using DMSO.

Air Pollutants, Occupational↗
PubMedDate not supplied

Determination of airborne isocyanate exposure: considerations in method selection.

To assess worker isocyanate exposures in a variety of processes involving the manufacture and use of surface coatings, polyurethane foams, adhesives, resins, elastomers, binders, and sealants, it is important to be able to measure airborne reactive isocyanate-containing compounds. Choosing the correct methodology can be difficult. Isocyanate species, including monomers, prepolymers, oligomers, and polyisocyanates, are capable of producing irritation to the skin, eyes, mucous membranes, and respiratory tract. The most common adverse health effect is respiratory sensitization, and to a lesser extent dermal sensitization and hypersensitivity pneumonitis. Furthermore, isocyanate species formed during polyurethane production or thermal degradation may also produce adverse health effects. Isocyanate measurement is complicated by the fact that isocyanates may be in the form of vapors or aerosols of various particle size; the species of interest are reactive and therefore unstable; few pure analytical standards exist; and high analytical sensitivity is needed. There are numerous points in the sampling and analytical procedures at which errors can be introduced. The factors to be considered for selecting the most appropriate methodology for a given workplace include collection, derivatization, sample preparation, separation, identification, and quantification. This article discusses these factors in detail and presents a summary of method selection criteria based on the isocyanate species, its physical state, particle size, cure rate, and other factors.

Air Pollutants, Occupational↗
PubMed2005

Isocyanates, polyurethane and childhood asthma.

Isocyanates are the most prominent and well-studied cause of occupational asthma. Over the decades, airborne isocyanates have been regulated to extremely low levels in the workplace, some of the lowest for any organic compound. Yet the incidence of isocyanate-induced occupational asthma remains high and the role of dermal exposure in disease etiology is only slowly being recognized. Almost completely overlooked is the potential relationship between isocyanates in consumer products and increasing prevalence of asthma in the general population, especially children. The steady rise in asthma over the past decades points strongly to a potential role of environmental exposures in its development. Imbalances in the immune system favoring respiratory diseases have been linked to biological and chemical stressor exposures early in life. Evidence for the presence of isocyanates in many polyurethane-containing materials, especially polyurethane foams, is presented as a possible contributor to the increase in asthma. Polyurethane foam is ubiquitous in western societies and used in bedding, furniture, automobile seats, footwear, etc., and numerous medical materials. Theoretical, epidemiologic, experimental and clinical evidence of a role for isocyanates and polyurethanes in the genesis of non-occupational allergy and respiratory disease are reviewed. These data all point to the urgent need for additional research on the links between isocyanates, polyurethanes and the role of the skin in non-occupational asthma.

Adult↗
PubMed2001

Occupational hypersensitivity pneumonitis due to isocyanates: mechanisms of action and case reports in Japan.

Isocyanates are very useful chemicals, and these are important for our daily life. Various products, especially urethane resin, are made from these chemicals. There is no substitute for isocyanates at the present. Isocyanates are patent agents to provoke immunological responses. This article deals with the case reports of hypersensitivity pneumonitis (HP) induced by isocyanates in Japan. It is said that HP is one of the rare diseases induced by isocyanate with very low frequency so far in the world. Certainly there are rare cases of isocyanate-HP also in Japan, but these are the cases only in large enterprises that pay attention to their working places. In Japan, there are several cases of isocyanate-induced HP, which happened in minor enterprises such as those with less than 50 workers. In clinical appearance, there are few conflicts with Western studies. The best choice for sensitized people is isolation from working places. It is important for the workers to understand the diseases. In these days, several tests for diagnosis are developed. It is indispensable to put these tests for prevention of these diseases and improvement of their working places.

Adult↗
PubMed2005

Asthma induced by isocyanates: a model of IgE-independent asthma.

Developments in the understanding of causes and natural history of asthma induced by isocyanates may allow improved preventive strategies for occupational asthma (OA), and may also lead to improved understanding of mechanisms involved in IgE-independent nonoccupational asthma. Studies of genetic markers in OA induced by isocyanates suggest that HLA class II genes, glutathione S-transferase and NAT1 genotypes may predispose to development of this type of OA. Specific IgE antibodies against isocyanates are not always found in subjects with OA caused by isocyanates, leading most researchers to consider this type of OA, as a model of IgE-independent asthma. Evidence for cell-mediated immunity in OA induced by isocyanates has been provided by bronchoalveolar lavage, bronchial biopsy and induced sputum studies. The pathology of this type of asthma is similar to that of nonoccupational asthma, with cells such as eosinophils and T lymphocytes that exhibit signs of activation, and with thickening of the reticular layer of the basement membrane. Animal studies have shown that isocyanate asthma is driven primarily by CD4+ T cells and is dependent upon the expression of Th2 cytokines. However, animal models are not always reflective of human responses. OA induced by isocyanates similarly to nonoccupational asthma, is a multifactorial condition, and it is likely that complex gene-environment interactions play a role. Better understanding of these interactions is important for affected workers, and also has potential relevance for nonoccupational asthma.

Animals↗
PubMedDate not supplied

Asthma due to isocyanates: a mail survey in a 1% sample of furniture workers in the Veneto region, Italy.

To ascertain the prevalence and risk factors in isocyanate asthma, we made a mail survey in a sample of workers in the wooden furniture industry, which uses large quantities of isocyanate-paints. Firms making up the initial sample, chosen from a register in the Veneto region, were asked to cooperate in the study. The study population, selected from the respondent firms, consisted of 1,430 subjects (about 2% of the parent population). Each subject received a self-administered questionnaire on respiratory symptoms and occupational history; this was mailed to his/her workplace. Completed questionnaires were returned by 730 subjects, who made up 51% of the population under examination (about 1% of the parent population). Fifteen subjects had suffered their first attack of asthma while in their present job: of these 7 were among the 121 who used paints (5.8% prevalence), and 8 were among the 609 who had no exposure (1.4% prevalence). The risk of asthma in the former group was therefore almost 5 times the risk in the latter. This result, however, is probably an underestimation because of the cross-sectional design of our study; at the time of study many asthmatics had already left their factory. There was a dose-response relationship between asthma and the length of exposure to isocyanates, the prevalence increasing from 2.2% in subjects with less than 20 years to 27.3% in workers with over 20 years' exposure. Lower prevalence of isocyanate asthma was found in the larger firms, where airborne exposure to isocyanate was believed to be lower. The continuous mode of exposure increased the risk of developing symptoms of asthma rather than intermittent acute exposure to high concentrations of isocyanates. Among painters, the prevalence of asthma ranged from 7.1% in non-smokers to 2.9% in smokers. As smoking appears to increase IgE production, a nonallergic mechanism may underlie isocyanate-induced occupational asthma.

Asthma↗
PubMed2006

Determination of airborne isocyanates.

Isocyanates are important in industrial hygiene and workplace monitoring. Owing to their severe acute toxicity and sensitizing properties, analytical methods with high sampling efficiency and sensitivity in the low ppb to ppt range are required. The reactivity of isocyanates necessitates initial derivatization with nucleophilic agents--usually amines--for stabilization and enrichment; this is often followed by chromatographic separation with spectroscopic, electrochemical, or mass spectrometric detection. Sampling strategies for airborne isocyanates comprise active, i.e. pumped, or passive, i.e. diffusive, methods; the method selected depends on the application. Whereas active methods rely mainly on impingers, reagent-coated filters, or sampling tubes, passive samplers make use of reagent-coated filters, the surface of which is connected to the air sample by diffusion channels. Because airborne isocyanates are prone to occur in different forms, i.e. as vapors, as aerosols, or adsorbed on particulate matter, denuder sampling has been introduced, thus enabling simultaneous collection of gaseous and aerosol isocyanates. The first part of this review summarizes chemical methods and reagents which have been introduced for derivatization of airborne isocyanates. The advantages and drawbacks of the individual derivatization procedures and their combination with different detection principles are evaluated. In the second part, the most recent developments in air sampling for isocyanates, with special focus on diffusive sampling, are reviewed and critically discussed.

Journal Article↗
PubMed1977

Active site specific inactivation of chymotrypsin by cyclohexyl isocyanate formed during degradation of the carcinostatic 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea.

Prolonged incubation of 1-(2-chloroethyl)-3-([1-14C]cyclohexyl)-1-nitrosourea with chymotrypsin resulted in covalent modification and concomitant inactivation of chymotrypsin via degradation of the nitrosourea to form cyclohexyl isocyanate. Cyclohexyl isocyanate was shown to be an active-site-specific inactivator of chymotrypsin. A cyclohexyl isocyanate to enzyme molar ratio of 0.63 was required to produce 50% enzyme inactivation, thus demonstrating the high specificity of inactivation. At 2.38 X 10(-4) M chymotrypsin this near stoichiometric inactivation was not significantly affected by the presence of 1, 5, and 10 mM L-lysine. Degradation of an excess of 1-(2-chloroethyl)-3-([1-14C]-cyclohexyl)-1-nitrosourea in the presence of enzyme yielded 1.11 +/- 0.07 mol of covalently bound [14C]cyclohexyl moiety per mol of enzyme inactivated. Short-term incubation demonstrated that the nitrosourea neither inhibited nor protected the enzyme from cyclohexyl isocyanate inactivation. Treatment of chymotrypsin with less than stoichiometric amounts of cyclohexyl isocyanate or titration of the active-site serine with phenylmethanesulfonyl fluoride followed by in situ degradation of excess 1-(2-chloroethyl)-3-([1-14C]cyclohexyl)-1-nitrosourea resulted in a decreased amount of covalently bound 14C proportional to the extent of inactivation by these reagents prior to 14C labeling. These results strongly suggest that cyclohexyl isocyanate, whether added directly or generated by CCNU degradation, reacted almost exclusively with the active site of the enzyme. The extent of this inactivation indicates that 70% of the CCNU degraded in such a manner as to form cyclohexyl isocyanate.

Binding Sites↗
PubMed2005

Trichlorosilane isocyanate as coupling agent for mild conditions functionalization of silica-coated surfaces.

Despite the importance of the isocyanate group in chemistry, very few examples of isocyanate-modified silicas have been reported, and all of the strategies described so far led to partial or total hydrolysis or condensation of the isocyanate group. By synthesizing trichlorosilane isocyanate as the coupling reagent, we show that oxidized silicon wafers are successfully modified with the isocyanate group. Our method is achieved in mild conditions, at low temperature, without side-reactions and allows the formation of a self-assembled monolayer (SAM) of isocyanates. The isocyanate group then offers a flexible way to further functionalize silica substrates with different nucleophiles, due to its high and specific reactivity.

Journal Article↗
PubMed2006

Validation of a diffusive sampling method for airborne low-molecular isocyanates using 4-nitro-7-piperazinobenzo-2-oxa-1,3-diazole-impregnated filters and liquid chromatography-tandem mass spectrometry.

A diffusive sampling method for the determination of low-molecular isocyanates as their 4-nitro-7-piperazinobenzo-2-oxa-1,3-diazole (NBDPZ) derivatives using tandem mass spectrometry (MS/MS) after atmospheric pressure chemical ionisation (APCI) is presented. Isocyanic acid (ICA), methyl isocyanate (MIC), ethyl isocyanate (EIC) and phenyl isocyanate (PhIC) are collected on NBDPZ-impregnated polystyrene divinyl benzene (SDB) filter tapes. The method was validated for MIC, EIC and PhIC for concentrations between 0.5 and 50 ppb at relative humidity (RH) conditions from 10 up to 90%. Validation was carried out by active sampling using 1-(2-methoxyphenyl)piperazine (2-MP) as derivatising agent. Sampling periods applied were between 15 min and more than 8 h. The sampling rates were determined to be 21.0 mL/min for MIC with a relative standard deviation (RSD) of 9.0% for 184 samplers, 15.6 mL/min for EIC (RSD 11.6%; N = 154) and 11.5 mL/min for PhIC (RSD 8.4%; N = 87). The limits of quantification were 1.4 ppb for MIC and 1.3 ppb for EIC and PhIC applying 15 min sampling periods. Owing to high background signals, isocyanic acid could only be determined when it was present in concentrations in the high ppb range.

Air↗
PubMed2003

Isocyanates of N alpha-[(9-fluorenylmethyl)oxy]carbonyl amino acids: synthesis, isolation, characterization, and application to the efficient synthesis of urea peptidomimetics.

The Curtius rearrangement of Fmoc-amino acid azides 1 was carried out in toluene by refluxing the solution for 30 min. The resulting isocyanates 2 have been isolated as crystalline solids and are fully characterized by IR, (1)H NMR, (13)C NMR, and mass spectra. They are found to be stable for several months when stored at 4 degrees C. The acyl azides of Asp, Glu, Ser, Tyr, and Lys with side-chain protection having tert-butyl, benzyl, and Boc groups were also converted to the corresponding isocyanates 2h-m. The rearrangement of Fmoc-amino acid azides in toluene to isocyanates 2 under microwave irradiation was also accomplished. The direct exposure of solid azides to microwaves for 60 s led to the completion of the rearrangement. The resulting isocyanates, after recrystallization, were found to be analytically pure. The scale-up of the rearrangement, under microwave irradiation as tested up to 0.75 mol, posed no problems and led to the isolation of the isocyanates in 91-96% yield. The utility of isocyanates as building blocks in the synthesis of urea peptides 4 is demonstrated. Further, the coupling of isocyantes 2 directly with N,O-bis(trimethylsilyl) derivatives of amino acids 6 resulted in urea peptide acids 7 with good yield in high purity. Thus, the synthesis of urea peptide acids 7d-g containing Asp, Glu, Ser, and Tyr with a free side-chain functional group have been carried out.

Amino Acids↗
PubMed2000

Isocyanate-specific hemoglobin adduct in rats exposed to 4, 4'-methylenediphenyl diisocyanate.

4,4'-Methylenediphenyl diisocyanate (MDI) is the most important of the isocyanates used as intermediates in the chemical industry. Among the main types of damage after exposure to low levels of MDI are lung sensitization and asthma. Protein adducts of MDI might be involved in the etiology of sensitization reactions. It is therefore necessary to have sensitive and specific methods for monitoring the isocyanate exposure of workers. To date, urine metabolites or protein adducts have been used as biomarkers in workers exposed to MDI. However, with these methods it is not possible to determine if the biomarkers result from exposure to MDI or to the parent aromatic amine 4,4'-methylenedianiline (MDA). This work presents a procedure for quantitating isocyanate-specific hemoglobin adducts. Blood proteins are used as markers of exposure and possibly as markers of dose size for the modifications of macromolecules in the target organs where the disease develops. For the quantitation of hemoglobin adducts, N(1)-[4-(4-isocyanatobenzyl)phenyl]acetamide (AcMDI) was reacted with the tripeptide valyl-glycyl-glycine and with valine yielding N-[4-(4-acetylaminobenzyl)phenyl]carbamoyl]valyl-glycyl-glycine and N-[4-[4-(acetylaminobenzyl)phenyl]carbamoyl]valine, respectively. N-[4-[4-(Acetylamino-3,5-dideuteriobenzyl)-2, 6-dideuteriophenyl]carbamoyl]valine was synthesized from valine, as was N(1)-[4-(4-isocyanato-3,5-dideuteriobenzyl)-2, 6-dideuteriophenyl]acetamide, for use as an internal standard. These adducts were cleaved in 2 M HCl to yield the corresponding hydantoins, 3-[4-(4-aminobenzyl)phenyl]-5-isopropyl-1, 3-imidazoline-2,4-dione (MDA-Val-Hyd) and 3-[4-(4-amino-3, 5-dideuteriobenzyl)-2,6-dideuteriophenyl]-5-isopropyl-1, 3-imidazoline-2,4-dione, respectively. In globin of rats exposed to MDI, MDA-Val-Hyd could be found in a dose-dependent manner. The adduct was identified by HPLC/MS/MS and quantified by GC/MS after derivatization with heptafluorobutyric anhydride. The amount of MDA-Val-Hyd found after acid hydrolysis of globin at 100 degrees C is about 12 times larger than the sum of N-acetyl-4, 4'-methylenedianiline (AcMDA) and MDA obtained from mild base hydrolysis of hemoglobin. The MDA-Val-Hyd is an isocyanate-specific adduct. MDA and AcMDA released after mild base hydrolyses result most likely from a sulfinamide adduct which is a typical adduct of arylamines. According to these results, higher amounts of isocyanate adducts than arylamine adducts should be expected in workers exposed to isocyanates.

Acetanilides↗
PubMed1995

The effects of benomyl and its breakdown products carbendazim and butyl isocyanate on the structure and function of tracheal ciliated cells.

The effects of the fungicide benomyl and its breakdown products, carbendazim and butyl isocyanate, were examined on canine tracheal epithelial tissue in primary culture. Changes in ciliary frequencies were monitored with an optical spectrum analysis system. Serial dilutions of the test compounds were prepared in 100% corn oil and applied to the cell cultures for intervals up to 6 hours and frequencies measured at intervals of 15 minutes to 1 hour. Benomyl and butyl isocyanate caused concentration-dependent decreases in ciliary beat frequency. Benomyl at 300 micrograms/ml (3 mM) caused ciliostasis within 75 minutes of exposure. Butyl isocyanate at a molar concentration three times lower than benomyl (1 mM) caused a similar response, although within 30 minutes. The IBC50 for benomyl was 0.75 mM, while for butyl isocyanate it was 0.52 mM. Carbendazim caused a moderate decrease in frequency over a 6 hour exposure period. Benomyl caused moderate to severe swelling of the mitochondria of ciliated epithelial cells with other cell organelles appearing normal. Butyl isocyanate did not cause any noticeable effect on cell ultrastructure and the apparently low rate of penetration of carbendazim into cells made it impossible to obtain an effect which justified ultrastructural analysis. It appears, at least for benomyl and butyl isocyanate, that while the physiological effect of these two compounds (inhibition of ciliary beat) is the same, the sites of action in the cell may be different.

Animals↗
PubMed2004

Isocyanate exposures in autobody shop work: the SPRAY study.

Isocyanates, known to cause respiratory sensitization and asthma, are widely used in automotive refinishing where exposures to aliphatic polyisocyanates occur by both inhalation and skin contact. The work reported here, the characterization of isocyanate exposure in the autobody industry, was part of an epidemiologic study of workers in 37 autobody shops in Connecticut. This article describes workplaces, tasks, and controls, and outlines the frequency, duration, and intensity of isocyanate exposures. Personal air samples taken outside of respirators had median concentrations of 66.5 microg NCO/m3 for primer, 134.4 microg (NCO)/m3 for sealer, and 358.5 microg NCO/m3 for clearcoat. Forty-eight percent of primer, 66% of sealer, and 92% of clearcoat samples exceeded the United Kingdom Health and Safety Executive guideline for isocyanate, though none exceeded the National Institute for Occupational Safety and Health (NIOSH) recommended exposure limit for monomer. Nonisocyanate-containing primers and sealers are used in more than half the shops, but nonisocyanate clearcoats are rare. Eighty-two percent of personal samples taken within a spray booth exceeded the U.K. guideline: 81% of those in downdraft spray booths, 74% in semidowndraft booths, and 92% in crossdraft booths. Only 8% of shops reported that spraying is done exclusively in spray booths. All painters wore some type of respirator. In 30% of shops, painters used supplied air respirators; the rest relied on half face organic vapor cartridge respirators with N95 overspray pads. All shops provided some type of gloves, usually latex, not recommended for isocyanate protection. Despite improvements in autobody shop materials, practices, and controls, there are still opportunities for substantial exposures to isocyanates.

Air Pollution, Indoor↗
PubMed2003

Need for monitoring nonspecific bronchial hyperresponsiveness before and after isocyanate inhalation challenge.

BACKGROUND: Specific and nonspecific bronchial responsiveness may decline or disappear after cessation of exposure in the workplace in patients with occupational asthma, leading to false-negative specific inhalation challenge (SIC) results. METHODS: Twenty-two patients with suspected diisocyanate-induced asthma were studied. SIC with diisocyanates (toluene diisocyanate [TDI] or hexamethylene diisocyanate [HDI]) was carried out in a 7-m(3) dynamic chamber up to a maximum concentration of 19 parts per billion for 120 min. Methacholine inhalation challenges were performed before and 24 h after SIC with TDI or HDI. Patients who did not show an asthmatic reaction after SIC but had a greater than twofold reduction in provocative concentration of methacholine causing a 20% fall in FEV(1) (PC(20)) after the first isocyanate challenge underwent a second isocyanate SIC 2 days later. RESULTS: The first SIC with isocyanates elicited an asthmatic reaction in 13 patients (59%). In five patients who did not show an asthmatic reaction after the first SIC, PC(20) exhibited more than a twofold reduction. In three of the five patients, a second SIC with isocyanates elicited an immediate positive asthmatic reaction. Therefore, 3 of 16 patients (19%) were ultimately shown to have bronchial responsiveness to isocyanate; occupational asthma was demonstrated due to post-SIC monitoring of bronchial hyperresponsiveness to methacholine. CONCLUSION: PC(20) should be systematically assessed before and after SIC with isocyanates in the absence of significant changes in FEV(1) during SIC to avoid false-negative results.

Adult↗
PubMedDate not supplied

Immunologic aspects of isocyanate asthma: IL-1 beta, IL-3, IL-4, sIL2R, and sICAM-1.

This pilot study investigated serum levels of cytokines and soluble receptors during five positive and five negative isocyanate inhalational challenges. Serum was obtained from 10 individuals with symptoms compatible with isocyanate asthma before isocyanate challenge and the day following their maximal change in pulmonary function after isocyanate challenge. Serum levels of interleukin 1 beta, interleukin 3, interleukin 4, soluble interleukin 2 receptor, and soluble intercellular adhesion molecule 1 were measured and compared. Interleukin 1 beta, interleukin 3, and interleukin 4 were not detected. The mean soluble interleukin 2 receptor and soluble intercellular adhesion molecule 1 levels were not statistically different before and after challenge or between groups. In summary, the cytokines studied are not detectable in peripheral blood during isocyanate inhalation challenge; soluble interleukin 2 receptor and soluble intercellular adhesion molecule 1 are both detectable but do not change significantly after a positive isocyanate challenge.

Administration, Inhalation↗
PubMed1989

Isocyanate exposure and hypersensitivity pneumonitis--report of a probable case and prevalence of specific immunoglobulin G antibodies among exposed individuals.

A car painter experienced three episodes of a hypersensitivity pneumonitis-like disease after exposure to two-component acrylic lacquers with hexamethylene diisocyanate (HDI) as the curing agent. High titers of HDI-specific immunoglobulin (Ig) G antibodies were found in the patient's serum by means of enzyme-linked immunosorbent assay (ELISA). In the ELISA, 5 to 10% of the sera from 455 isocyanate-exposed but asymptomatic workers were positive, depending on the criterion used for a positive test, whereas 0% of the sera from 157 unexposed referents was found to be positive. Among 10 subjects with isocyanate-induced asthma and isocyanate-specific IgE antibodies, 50% had specific IgG. It was concluded that the presence of isocyanate-specific IgG antibodies in serum is correlated with isocyanate exposure rather than with symptoms of isocyanate-induced disease.

Adult↗
PubMed1997

Airway isocyanate-adducts in asthma induced by exposure to hexamethylene diisocyanate.

OBJECTIVES: The clinical features, airway histology, and detection of hexamethylene diisocyanate (HDI) protein adducts in endobronchial biopsies from a patient with HDI asthma are described. METHODS: Isocyanate asthma was diagnosed by history, methacholine challenge, and workplace HDI challenge. Bronchoscopy was performed 24 h after challenge and immunohistochemical staining was performed. RESULTS: Airway biopsies obtained at bronchoscopy demonstrated inflammatory changes typical for asthma, including increased airway eosinophils and T cells. Immunohistochemical staining with specific anti-HDI antibodies demonstrated the presence and localization of HDI adducts in human bronchial biopsies. CONCLUSIONS: These studies confirm epithelial exposure to HDI following workplace challenge and demonstrate the feasibility of detecting and localizing isocyanate adducts in human lung tissue. Identifying and characterizing the airway macromolecules to which isocyanates bind in vivo are probably crucial to the understanding of how isocyanates cause sensitization and asthma. The ability to detect isocyanate adducts may also help characterize isocyanate exposure patterns and exposure-disease relationships.

Adult↗