Occupational Asthma Reference

Fernández-Nieto M, Quirce S, Fraj J, del Pozo V, Seoane C, Sastre B, Lahoz C, Sastre J, Airway inflammation in occupational asthma caused by styrene, J Allergy Clin Immunol, 2006;117:248-250,
(Plain text: Fernandez-Nieto M, Quirce S, Fraj J, del Pozo V, Seoane C, Sastre B, Lahoz C, Sastre J, Airway inflammation in occupational asthma caused by styrene, J Allergy Clin Immunol)

Keywords: styrene, challenge, NSBR, case report

Known Authors

Joaquin Sastre, Fundacion Jimenez Diaz, Madrid Joaquin Sastre

Santiago Quirce, Madrid Santiago Quirce

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Styrene or phenylethylene has rarely been reported as a causative agent of occupational asthma. This volatile monomer is widely used in the production of polymers, copolymers, and reinforced plastics and is a reactive solvent in the manufacture of unsaturated polyester resins. Styrene is known as an irritant to the skin and mucous membranes and has been associated with dysfunction of the central nervous system. Workers in auto body shops may be exposed to styrene, because they use polyester resins in paints and car putty.

A 31-year-old man, a nonatopic and nonsmoker with persistent asthma, was referred for evaluation to the outpatient allergy clinic of our hospital. He had worked as a painter in an auto body shop for 4 years on a regular 8-hour shift during the day. He did not wear any protective equipment. During the last year, he had experienced sneezing, nasal discharge, ocular itching, and nasal stuffiness as well as dyspnea, dry cough, and wheezing when working. Asthma symptoms were more intense at the end of the work shift and at night, and he remained symptom-free during holidays and days off work. He handled paints containing hexamethylene diisocyanate (HDI) and polyester resins and hardeners that included in their composition styrene at a concentration of 10% to 25%, as disclosed by product labels and material data safety sheets.

He was evaluated 4 months after he had left his job because of asthma symptoms. After obtaining written informed consent, 3 single-blind specific inhalation challenges (SICs) were performed in a 7-m3 challenge chamber on separate days. This chamber is made of lacquered stainless steel (Telstar Projects SA, Madrid, Spain) and equipped with vacuum exhaust and high-efficiency particle arrest filtration. On visit 1, PC20 was measured, and sputum induction was performed. On visit 2, the patient painted placebo solution (polyol) with a brush onto a cardboard for 5 minutes. Spirometry was performed at 5, 10, 20, 30, 40, and 60 minutes after the inhalation challenge. From that moment, peak expiratory flow and FEV1 were measured hourly with a computerized flowmeter (Amos, Jaeger, Germany) for 24 hours after challenge, respecting sleeping time. On visit 3, the patient underwent a SIC with HDI. Twenty-four hours later, on visit 4, methacholine inhalation test and sputum induction were performed again. Three days later, on visit 5, the patient painted the styrene solution (20 mL) on a cardboard for 4 minutes, and the following day, on visit 6, a methacholine inhalation test and sputum induction were performed.

Physical examination, blood tests, and spirometry results were normal. Specific IgE against diisocyanates measured in the patient's serum was negative. Specific IgE against styrene was assayed in duplicate by ELISA, using a concentration of 20 µg/mL and serum dilution series starting from 1:2 as described elsewhere,5 and was also negative. Sputum was induced by hypertonic saline inhalation and processed as previously described (both with and without dithiothreitol).6 Sputum samples were analyzed using flow cytometer scan cytometry (FACSCalibur flow cytometer; Becton Dickinson, San José, Calif). mAbs (Pharmingen, San Diego, Calif) used to identify cells were CD19, CD3, CD4, CD8, CD16, CD45, CCR3 (B and T lymphocytes, neutrophils, and eosinophils), CD63, and CDw125 (activated basophils).

At baseline (visit 1), PC20 methacholine was 1 mg/mL. On visit 2 (sham exposure), no significant changes in FEV1 were observed over the next 24 hours. On visit 3, SIC with HDI at a concentration of 15 ppb for 120 minutes elicited no reaction. No significant changes in FEV1, PC20 methacholine, or cell counts in induced sputum were observed 24 hours after the HDI challenge. On visit 5, the styrene challenge elicited an isolated late asthmatic response, with a maximum fall in FEV1 of 22% 11 hours after the provocation test. An increase in sputum eosinophils from 0.02 × 106 to 0.43 × 106 cells/mL and a striking increment of activated basophil counts in induced sputum were observed 24 hours after styrene SIC, but no significant changes were observed in PC20 methacholine. The results of induced sputum analysis by flow cytometry did not vary with or without dithiothreitol.

Three subjects with suspected occupational asthma underwent the same challenge protocol with styrene, and no relevant changes in FEV1 or PC20 methacholine were observed. The increase in eosinophil and basophil counts in sputum after styrene SIC in the patient, as well as the negative results obtained with exposure to placebo and HDI, support the specificity of the airway reaction to styrene. A rise in eosinophil counts in sputum greater than 0.26 × 106 cells/mL after SIC or greater than 2% after exposure at work are considered to be clinically significant. An increase in basophil counts in induced sputum has been found in atopic subjects with asthma9 and subjects with occupational asthma10 after SIC. Interestingly, the number of sputum basophils correlated with airway hyperresponsiveness to methacholine.9

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