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PubMed1989

Immunologic specificity of isocyanate-induced IgE antibodies in serum from 10 sensitized workers.

A procedure for the preparation of RAST disks used to assay isocyanate-specific IgE antibodies was developed. The outcome of the RAST was found to be strongly dependent on how the isocyanate test antigen was synthesized. Specific IgE from selected workers with isocyanate asthma reacted optimally to conjugates with less than or equal to 10 isocyanate molecules bound per molecule of human serum albumin. Further haptenization resulted in decreased specific binding and increased nonspecific binding because of high levels of total IgE. The hapten and carrier specificity of isocyanate-induced IgE antibodies were studied by direct RAST and RAST inhibition. The existence of new antigenic determinants related to both the isocyanate hapten and the carrier could be demonstrated. It was important to use a test antigen prepared from the same isocyanate as that to which the worker had been exposed, since the cross-reactivity between different isocyanate haptens was partial and varied from one patient to another. It was confirmed that isocyanate-specific IgE antibodies can be demonstrated only in a subgroup of workers with isocyanate-related bronchial asthma.

Antibody Specificity↗
PubMed1997

Outcome determinants for isocyanate induced occupational asthma among compensation claimants.

OBJECTIVES: To compare the outcome of occupational asthma (OA) induced by isocyanates in Ontario (where a surveillance programme for exposed workers has been in place for over 15 years), with the outcome of OA induced by other work agents. METHODS: Compensated OA claims during the period 1984-88 in Ontario were retrospectively reviewed in a standardised way. RESULTS: 136/235 compensated claims were attributed to isocyanates. Compared with other causes of OA, those attributed to isocyanates had a shorter latent period before onset (5.9 v 7.9 years, P < 0.05), shorter duration of symptoms before diagnosis (2.0 v 3.0 years, P < 0.05), and less associated atopy (43% v 58%, P < 0.05). Outcome at a mean of 1.9 years after initial assessment was significantly better in those with OA induced by isocyanates; 73% cleared or improved v 56% with other causes of OA (P < 0.05). Ten subjects with OA induced by isocyanates stayed at the same work; none cleared and four had worsened at follow up. A better outcome in OA induced by isocyanates was associated with early diagnosis (P < 0.05), and early removal from isocyanates after the onset of asthma. CONCLUSIONS: The outcome in the group with OA induced by isocyanates is similar to previous follow up studies. However, it is better than the outcome in our comparison group with OA due to other causes, perhaps because of earlier diagnosis in the group with OA induced by isocyanates. This may be attributable to the medical surveillance of workers exposed to isocyanates in Ontario, either directly from the surveillance assessments, or indirectly by increasing awareness of the condition.

Adult↗
PubMed1992

Workers' exposure to isocyanates.

A model of exposure to isocyanates, based on knowledge of industrial processes and starting materials and the results of industrial hygiene surveys, is proposed. This model of exposure suggests the concentration and physical form of airborne isocyanate monomers and oligomers. A new sampling and analytical system was developed that is capable of determining the physical and chemical characteristics of occupational exposure to a variety of aliphatic and aromatic isocyanates as required by the exposure model. The sampling system consisted of a dual-filter 37-mm cassette, in which the first filter captured aerosol phase contaminants and the second captured vapor phase isocyanates through derivatization with 9-(N-methylaminomethyl) anthracene (MAMA). Urea derivative recovery by the sampling system, isocyanate-MAMA reactivity, and linearity of the calibration curve were evaluated in the laboratory. The practicality of the system was evaluated during field trials. Sampling times are reduced to 15 min, and the detection limit for TDI, HDI, and MDI was 1.0 micrograms/m3. A partial validation of the new sampling system was performed for HDI vapor by comparison to a standard method in field trials and for TDI vapor in a controlled test atmosphere. The analytical system may also be used to measure the concentration of oligomeric isocyanates. Airborne concentrations of isocyanates were measured in two foam plants, nine paint shops, and two foundries to verify the usefulness of the model. Exposure in foam plants was predominantly to gaseous monomeric isocyanates. Exposure to oligomer isocyanates was higher than expected in paint shops. Both monomer and oligomer isocyanates were undetectable in foundries.

Air Pollutants, Occupational↗
PubMed1975

Inhibition of rat liver DNA polymerase by nitrosoureas and isocyanates.

The effects of 1,3-bis(2-chloroethyl)-1-nitrosourea, 1-(2-chloroethyl)-3-cyclohexl-1-nitrosourea, and 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea on two nonmitochondrial DNA polymerases (I and II) purified from rat liver and hepatoma were examined. The activity of DNA polymerase I was not altered by treatment with any of the nitrosoureas or the corresponding isocyanates, 2-chloroethyl isocyanate and cyclohexyl isocyanate. Incubation of DNA polymerase II with the nitrosoureas (1 mM) inhibited its enzymatic activity 30 to 45%. DNA polymerase II was inhibited 75 and 90% by 1.mM 2-chloroethyl isocyanate and cyclohexyl isocyanate, respectively. The nitrosoureas appear to exert their inhabitory action on the enzyme (DNA polymerase II) rather than on the DNA template. Pretreatment of the enzyme increased the degree of inhibition by 1 mM nitrosourea (50 to 60% inhibition) or 2-chloroethul isocyanate (greater than 90% inhibition), whereas pretreatment of the DNA template did not enhance the inhibitory effect. The three nitrosoureas are equally effective as inhibitors of DNA polymerase II. 2-Chloroethyl isocyanate and cyclohexyl isocyanate are better inhibitors than are the nitrosoureas. Since further decomposition products of the isocyanates, 2-chloroethylamine and cyclohexylamine, do not inhibit DNA polymerase II, we conclude that the isocyanates, which are decomposition products of the nitrosoureas, are the active inhibitors of the enzyme.

Animals↗
PubMed1983

Immunologic cross-reactivity between different albumin-bound isocyanates.

Sera of six workers with conclusive evidence for IgE-mediated sensitization to isocyanates were used for evaluation of immunologic cross-reactivities among eight different isocyanate-protein conjugates. In all cases RAST and/or skin-test investigations revealed the presence of IgE antibodies reacting specifically with HSA conjugated with those isocyanates to which workers were exposed as well as with other isocyanates with which they had not been in contact. By the RAST inhibition technique, moderate to strong mutual cross-reactivities between all tested isocyanate-HSA conjugates--even between aromatic and aliphatic ones--could be demonstrated in tests with five sera. The magnitudes of cross-reactivities differed, however, from one patient to another. One serum contained IgE antibodies that were almost completely specific to TDI-HSA; with this serum only weak cross-reactivities with other isocyanate conjugates could be demonstrated. These results indicate the predominance of closely related antigenic determinants in HSA conjugated with different isocyanates. The common antibody-binding regions are obviously recognized to different extents by antibodies of clinically sensitized workers, indicating individual differences in specificities and avidities of antibody populations. Nearly complete lack of IgE binding of ovalbumin-bound TDI in RAST and RAST inhibition indicates carrier-specific antigenicity of isocyanate-protein conjugates. In addition, since unmodified HSA did not bind IgE, antigenic determinants of the conjugates studied should be predominantly formed by the isocyanate-protein bond regions and concurrently by neighboring amino acid residues of the HSA molecule.

Adult↗
PubMed1995

Hypersensitivity pneumonitis (extrinsic allergic alveolitis) induced by isocyanates.

BACKGROUND: Chemical-induced hypersensitivity pneumonitis has been so far rarely described. The purpose of this study was to find out whether hypersensitivity pneumonitis is a common disorder in isocyanate workers. METHODS: Company physicians' case histories of 1780 isocyanate workers were evaluated. In 16 subjects suspected of having isocyanate-induced hypersensitivity pneumonitis, chest x-ray films were made; levels of IgE and IgG antibodies to isocyanate-human serum albumin were estimated; conjugates and isocyanate challenge tests, bronchoalveolar lavage fluid analyses, and/or lung histologic investigations were performed. RESULTS: Each of the 14 study patients who had hypersensitivity pneumonitis had work-related dyspnea and fever occurring several hours after the start of work with isocyanates. Typical clinical findings were the reduction of lung diffusing capacity (n = 10), reticular or nodular lung patterns in the x-ray film (n = 9), and serum IgG antibodies specific to isocyanate-human serum albumin conjugates (n = 10). Restrictive ventilation patterns in the inhalation challenge tests (n = 5), lymphocytic and/or neutrophilic alveolitis seen in bronchoalveolar lavage fluid analyses (n = 7), and lymphohistiocytic patterns mostly associated with mild fibrosis in lung histology (n = 5) confirmed the diagnosis. CONCLUSIONS: Occupational exposure to isocyanate vapors and aerosols induces typical hypersensitivity pneumonitis in at least 1% of the isocyanate workers with symptoms. Diphenylmethane diisocyanate was found to be the main cause of this disorder.

Adolescent↗
PubMed1984

Evaluation of total isocyanate-in-air method using 1-(2-methoxyphenyl)piperazine and HPLC.

The United Kingdom Health and Safety Commission has set a 'common control limit' for workplace exposure to all isocyanates. This limit replaces the previous United Kingdom threshold limit values, which were set for just four species of monomeric isocyanate compounds. This new control limit is set at 20 micrograms of isocyanate group per cubic meter of air expressed as an eight-hour weighted average, and 70 micrograms of isocyanate group per cubic meter of air as a 10-minute weighted average. These new control limits make it necessary that analytical methods should be capable of measuring total isocyanate concentration, including monomers and prepolymers. A previously available method for determining isocyanate monomers using 1-(2-methoxyphenyl)piperazine with high performance liquid chromatography (HPLC) has been modified to measure both monomer and prepolymer. A dual detection system employing electrochemical and ultra-violet detectors is used to identify isocyanate-derived HPLC peaks which are then quantified by reference to a monomer standard, thus avoiding the necessity of isolating prepolymer standards. The total isocyanate-in-air concentration is then calculated from the total area of the isocyanate-derived HPLC peaks. The precision of the method is better than 10% over the range 35 to 140 micrograms(NCO)/m3 for a 10 min sample.

Air Pollutants↗
PubMed1989

Role of inhalation challenge testing in the diagnosis of isocyanate-induced asthma.

Results of isocyanate challenge tests performed on 63 workers referred with a diagnosis of probable isocyanate asthma between 1974 and 1988 were reviewed. Thirty (48 percent) had an acute episode of asthma with a greater than 20 percent decline in FEV1 following subirritant exposure to isocyanates. No difference in the frequency or type of respiratory complaints between isocyanate reactors and nonreactors was found. No differences in lung function results were present when comparing smoking and ex-smoking reactors and nonreactors. In never-smokers with complaints consistent with isocyanate-induced asthma, the presence of obstructive lung disease increased the likelihood that isocyanate-induced asthma was present. Bronchial responsiveness to methacholine occurred in nearly all isocyanate reactors but predicted isocyanate-induced asthma in only 68 percent of the workers. In nearly all cases of challenge-confirmed toluene diisocyanate (TDI)-induced asthma, a 15-min exposure to 20 ppb of the commercial TDI mixture (80:20 2,4:2,6) provoked asthma. Conversely, in the absence of an asthmatic response following exposure to this dose for this duration, a second exposure at this concentration for a longer time would be reasonable to confirm the absence of isocyanate-induced asthma. Among workers employed in the production of polyurethane foam and confirmed to have TDI-induced asthma by inhalation challenge to the different TDI isomers, there appeared to be increased airway reactivity to the 2,6 isomer. This may have relevance to the frequency and intensity of respiratory symptoms that workers with TDI-induced asthma develop in differing industrial settings.

Adult↗
PubMed2000

Qualitative assessment of isocyanate skin exposure in auto body shops: a pilot study.

BACKGROUND: Little is known about the extent of human isocyanate skin exposure in auto body shops and the effectiveness of personal protective equipment. Animal studies have suggested that skin exposure to isocyanates may be an important risk factor for respiratory sensitization leading to asthma. This study provides initial data on hexamethylene diisocyanate skin exposure in three auto body shops. METHODS: Three auto body shops of different size which use different paint systems were examined for the presence of aliphatic isocyanates on environmental surfaces and workers' skin and for breakthrough of personal protective equipment. Qualitative detection of contamination by isocyanates was conducted using a wipe-sampling technique. Assessment focused on the painters and their tasks, although other auto body repairers were also evaluated. RESULTS: Environmental surfaces such as painters' workbenches, spray equipment, and cleaning tools were found contaminated with isocyanates. Painters had frequent contact with contaminated surfaces, often without wearing gloves. Moderate to heavy contamination of some skin surfaces was found with painters from two of the three auto body shops. Latex gloves used for skin protection showed significant penetrations by isocyanates even after a single painting session. CONCLUSIONS: Contaminated environmental surfaces and skin exposure to isocyanates were documented in several auto body shops. Latex gloves were not adequate protection for workers using isocyanate paints. Further research which would better quantify skin exposure, and its potential relationship to respiratory sensitization and asthma is warranted.

Asthma↗
PubMed2002

Determination of isocyanates, aminoisocyanates and amines in air formed during the thermal degradation of polyurethane.

An air sampling method for the determination of isocyanates, aminoisocyanates and amines formed during the thermal degradation of polyurethane (PUR) is presented. The method is based on the collection of air samples using impinger flasks containing di-n-butylamine (DBA) in toluene with a glass fibre filter in series. Isocyanates are derivatized with DBA to urea derivatives, and amines are derivatized in a subsequent work-up procedure with ethyl chloroformate (ET) to carbamate esters. Amine, aminoisocyanate and isocyanate derivatives were characterized using liquid chromatography-time of flight mass spectrometry (LC-TOFMS) and liquid chromatography-chemiluminescent nitrogen detection (LC-CLND). Quantification was performed by LC-MS, monitoring molecular ions [MH]+ in the electrospray mode. The instrumental detection limits for amines, aminoisocyanates and isocyanates were in the ranges 30-40, 2-3 and 3-70 fmol, respectively. Thermal degradation products of PUR were observed in high concentrations during welding in district heating pipes and PUR-coated metal sheets. Eleven isocyanates, three amines and five aminoisocyanates were identified. The concentrations of isocyanates, aminoisocyanates and amines in samples collected in the smoke close to the welding spot were in the ranges 150-650, 4-290 and 1-70 ppb, respectively. In samples collected in the breathing zone, isocyanates and aminoisocyanates were observed in the ranges 9-120 and 4-19 ppb, respectively. The compounds were present in both gas and particle phases. Volatile compounds dominated in the gas phase, whereas less volatile compounds dominated in the particle phase. The method presented makes it possible to sample and determine amines and aminoisocyanates, in addition to isocyanates. The need to monitor these compounds is clearly illustrated by the high concentrations found during the thermal degradation of PUR.

Air Pollutants↗
PubMed1996

Development of a novel derivatization reagent for the sampling and analysis of total isocyanate group in air and comparison of its performance with that of several established reagents.

Analytical reference standards generally are not available for non-monomeric isocyanate species, making accurate identification and quantitation by high-performance liquid chromatography (HPLC) difficult. A successful derivatizing reagent must react rapidly with all isocyanate groups, the derivatized isocyanate must be detectable selectively and at very low levels, and the detector used for quantitation must give a response proportional to the number of derivatized isocyanate groups present. A novel derivatizing reagent, 1-(9-anthracenylmethyl)piperazine (MAP), was prepared in an attempt to achieve these goals. Derivatives were prepared by reacting five mono- and difunctional isocyanates with MAP and three other established isocyanate derivatizing reagents. These reagents included 1-(2-methoxyphenyl)piperazine (MOPP),9-(methylaminomethyl)anthracene (MAMA), and tryptamine (TRYP). The relative reactivities of MAP, MOPP, TRYP, and MAMA with phenyl isocyanate were found to be 100, 88, 30, and 25, respectively. Average molar absorptivities at the absorbance maxima +/- compound-to-compound variabilities were, for MAP: 1.47 x 10(5) +/- 3.50%; MAMA: 1.38 x 10(5) +/- 7.07%: and TRYP: 3.98 x 10(4) +/- 13.1%. Average fluorescence responses were, for MAP: 100 +/- 32.6%; MAMA: 41.0 +/- 58.8%; and TRYP: 2.27 +/- 15.6%. A comparison of MAP and MOPP ureas by HPLC/ultraviolet (UV)/electrochemical (EC) gave average responses for UV, EC, and EC/UV for MAP: 117 +/- 7.3%, 52.1 +/- 6.6%, and 0.447 +/- 10.7%, respectively; for MOPP: 24.3 +/- 62.5%, 76.7 +/- 28.5%, and 4.28 +/- 59.1%, respectively. The favorable performance of MAP warrants its further study as a reagent for the determination of total isocyanate group in air.

Air Pollutants, Occupational↗
PubMed2005

Glutathione protects human airway proteins and epithelial cells from isocyanates.

BACKGROUND: Glutathione (GSH), one of the major anti-oxidants of the lung, has been linked to the human response to isocyanate exposure. However, the ability of GSH to modulate key chemical reactions, thought to be central to the development of human isocyanate allergy, has not been directly analyzed under biologic exposure conditions. OBJECTIVE: To better understand the potential role of GSH in the response to occupational isocyanate exposure, we evaluated its effects on two processes thought to be involved in the development of isocyanate allergy, isocyanate-protein conjugation and epithelial cell toxicity. METHODS: The effects of GSH on (1) isocyanate conjugation with albumin, its major target in the airway fluid and (2) isocyanate-induced toxicity to human airway epithelial cell lines, A549 and NCI-H292, were tested using two different in vitro models. For protein conjugation studies, a newly described vapour exposure system was used to model the air/liquid interface at the surface of the epithelial fluid in the airways. Epithelial cell exposures were performed in fluid phase to mimic the in vivo exposure of airway cells covered by epithelial lining fluid. RESULTS: Reduced GSH prevented hexamethylene diisocyanate (HDI) conjugation to albumin in a dose-dependent manner, while oxidized GSH (GSSG) conversely increased conjugation rates. GSH levels equivalent to those found in normal human airway fluid (100 microm) provided >90% protection against HDI-protein conjugation when albumin was exposed to HDI vapour levels 10-fold above permissible occupational limits. Physiologic levels of GSH, but not GSSG, also reduced HDI toxicity to human airway epithelial cells in a dose-dependent manner, when present extracellularly, however, drugs that modulate intra-cellular GSH levels did not significantly alter isocyanate toxicity. CONCLUSIONS: Together with previously reported genetic and toxicity studies, the data suggest that airway GSH plays an important role in protection against HDI exposure and may help prevent the development of allergic sensitization and asthma.

Air Pollutants, Occupational↗
PubMed1997

Assessment of the relationship between isocyanate exposure levels and occupational asthma.

As part of a previous study, we identified Ontario cases of isocyanate-induced occupational asthma (OA) and the companies at which they worked. The Ontario Ministry of Labour maintained a computerized database including isocyanate air sampling determinations conducted by the Ministry. Within this database, we compared levels of isocyanate concentrations measured at 20 case companies [with compensated isocyanate asthma (OA) claims] with 203 noncase companies, based on air samples collected during the same 4-year period during which the OA claims arose. The proportion of case companies that were ever recorded as having a measured ambient isocyanate concentration of > or = 0.005 ppm was greater than that for noncase companies, for TDI users (43% vs 22%), and for MDI users (40% vs 27%). This reached conventional significance when combined across companies and isocyanate types (50% vs 25%; P < 0.05). This provides some evidence that facilities having OA claims have higher isocyanate exposures than do those without claims.

Air Pollutants↗
PubMed1994

Respiratory and other hazards of isocyanates.

Isocyanates are increasingly being used for manufacturing polyurethane foam, elastomers, adhesives, paints, coatings, insecticides, and many other products. At present, they are regarded as one of the main causes of occupational asthma. The large number of workers who are exposed to these chemicals have a concentration-dependent risk of developing chronic airway disorders, especially bronchial asthma. Different pathophysiologic mechanisms are involved. Immunoglobulin E (IgE)-mediated sensitization and irritative effects have been clearly demonstrated in both exposed subjects and animals. Presumably, neural inflammation due to neuropeptide release of capsaicin-sensitive afferent nerves is crucial. We collected data on 1780 isocyanate workers who had been examined by our groups. Of them 1095 (including subjects from outpatient departments) had work-related symptoms, predominantly of the respiratory tract. Specific IgE antibodies were found in 14% of the 1095 subjects. The methacholine challenge test was shown to be an inadequate predictor of the results of inhalative isocyanate provocation tests in workers and in asthmatic controls. Isocyanate (toluene diisocyanate TDI) air concentrations of 10 ppb (0.07 mg/m3) and 20 ppb (0.14 mg/m3), respectively, did not cause significant bronchial obstruction in the majority of previously unexposed asthmatics with bronchial hyperreactivity. IgG-mediated allergic alveolitis, a rare disease among isocyanate workers, was found in approximately 1% of the symptomatic subjects. Experimental studies exhibit dose-dependent toxic effects and give evidence for tachykinin-mediated bronchial hyperreactivity after exposure to isocyanates. The clinical role of genotoxic effects of isocyanates and their by-products demonstrated here in vitro and in vivo has yet to be clarified.

Air Pollutants, Occupational↗
PubMed2006

Increase in exhaled nitric oxide (eNO) after work-related isocyanate exposure.

UNLABELLED: The objective of this study was to evaluate the role of eNO changes post inhalative isocyanate challenge tests (DeltaeNO) with regard to specific asthmatic reactions and unspecific bronchial hyperresponsiveness (BHR) to predict clinical and subclinical responses of isocyanate workers. METHODS: 55 workers with isocyanate-related respiratory complaints (29 with BHR and 25 without BHR) underwent occupational-type challenge tests. We determined eNO before, during and up to 22 h after diagnostic isocyanate challenge. RESULTS: The 12 asthmatic responders (22%) in the isocyanate-challenge test showed the highest eNO changes 22 h after challenge as well as a significant association between these changes and BHR. There was a positive association between an eNO increase of > 50% and an asthmatic response when compared to nonresponders with an odds ratio of 6.1; 95% CI 1.4-26.3; P = 0.02. More than half of the employees with BHR (52%) but only 20% of those without BHR developed an eNO rise of > 50% after 22 h. Furthermore, a significant positive association was found between the combination of BHR plus eNO increase of 50% after 22 h and the maximum sRaw change (% of baseline value) during the period 0-22 h after isocyanate exposure. The combination of BHR and eNO increase of > 50% was also associated with clinical symptoms during specific challenge tests (cough, shortness of breath, and/or rhinitis). DISCUSSION AND CONCLUSIONS: An eNO increase 22 h post isocyanate challenge occurred in two-thirds of responders and in approximately half of nonresponders with BHR but only rarely in those without BHR. The combination of BHR and eNO increase in nonresponders may offer a new diagnostic tool to register subjects with an increased risk of developing occupational asthma. However, a large study group to perform follow-up investigations into this topic would be helpful to emphasize the importance of this finding.

Asthma↗
PubMed1983

Guinea pig respiratory response to isocyanates.

Exposure to some isocyanates (e.g., toluene diisocyanate) has been associated with development of respiratory sensitization. In this study, guinea pig respiratory response to protein conjugates of isocyanatoethyl methacrylate (IEM) and isocyanatoethyl propionate (IEP) was evaluated. Guinea pigs were exposed to daily induction exposures with an aerosol of bovine serum albumin (BSA) or BSA conjugated with IEM or IEP. After approximately 2 weeks significant increases in respiratory rate occurred in the guinea pigs exposed to the isocyanate conjugates. The number of animals responding was related to the degree of conjugation of isocyanate to protein. No response to unconjugated BSA was observed. The isocyanates conjugated to another carrier, guinea pig serum albumin (GSA), elicited responses. In guinea pigs responding to BSA-IEM, 0.01 ppm IEM monomer did not elicit responses; 0.1 to 0.4 ppm IEM vapor elicited responses similar to conjugates but which were delayed; 0.5 and 0.6 ppm induced irritation responses. An IEM polymer aerosol that contained less than 0.004% monomer did not elicit a response. These data suggest a response threshold. Guinea pig developing responses to either of the isocyanate conjugates displayed cross-reactions to challenge with the other. A conjugate of BSA with hexyl isocyanate (HI) did not induce cross-responses in guinea pigs reactive to BSA-IEM. Application of BSA-IEP or IEP monomer to the scratched skin of guinea pigs that responded by inhalation to BSA-IEP resulted in immediate wheal and flare responses not seen in unexposed animals. All of these findings suggest induction of Type I hypersensitivity (asthmatic) directed toward the isocyanate portion of the conjugate and not the protein.

Acrylates↗
PubMed1998

Specific IgE to isocyanates: a useful diagnostic role in occupational asthma.

BACKGROUND: Isocyanates are the most frequent cause of occupational asthma in industrialized countries. OBJECTIVE: We sought to investigate the utility of specific IgE measurement in the diagnosis of isocyanate-induced asthma. METHODS: Fifty-eight of 101 patients referred for investigation were diagnosed as having isocyanate-induced occupational asthma by means of history, serial peak flow records, and bronchial provocation tests. Specific IgE antibodies to toluene diisocyanate:human serum albumin (HSA), diphenylmethane diisocyanate:HSA, and hexamethylene diisocyanate: HSA were measured in all patients by Phadebas RAST. RESULTS: Twenty patients had a RAST ratio of 2 or greater to at least one isocyanate. Thirteen (28%) of the 46 patients with a positive provocation test response had a RAST ratio of 2 or greater, and nine (20%) had a RAST ratio of 3 or greater. Raising the RAST cut-off from 2 or greater to 3 or greater reduced its sensitivity but increased the specificity of the test to 100%. RAST measurement was most likely to be positive within 30 days of exposure. Serial measurements suggested that the half-life of the IgE antibodies was approximately 6 months. Evidence of cross-reactivity between isocyanate RAST responses was found in eight subjects. CONCLUSION: Specific IgE to isocyanates is a more specific than sensitive index of occupational asthma. With a RAST score of 3 or greater, it is wholly specific and therefore diagnostic of isocyanate-induced asthma. The sensitivity of specific IgE measurement is highest when blood is taken less than 30 days from last exposure, which is consistent with the observed half-life.

Adolescent↗
PubMed2003

Occupational allergic contact dermatitis in a company manufacturing boards coated with isocyanate lacquer.

Over a short period of time, there was an outbreak of work-related skin lesions among workers at a company producing flooring laminate boards, after the introduction of a water-repellent lacquer based on diphenylmethane-4,4'-diisocyanate (MDI). In 5 workers, patch testing was performed with a standard series, an isocyanate series and work-environmental products when indicated. 3 of the workers were tested with the lacquer, and contact allergy was found with concurrent reactions to 4,4'-diaminodiphenylmethane (MDA). 1 of the 3 workers also showed a simultaneous reaction to MDI, whereas 1 showed a positive reaction to dicyclohexylmethane-4,4'-diisocyanate (HMDI). Of the 2 individuals not tested with the lacquer, 1 reacted to both MDI and MDA, whereas the other reacted to a soap used at work. In 3 of 4 cases, the isocyanate reactions appeared after D3. Occupational contact with isocyanates should not exclusively be focused upon respiratory hazards, as this report shows that skin contamination probably increases the risk of developing contact allergy to isocyanates and isocyanate-related substances. When aiming at diagnosing contact allergy to isocyanates, it is desirable to perform a late reading, as positive reactions appear late. MDA appears to be a good marker for isocyanate hypersensitivity.

Adult↗