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Occupational and Environmental Lung Disease |

Occupational Asthma Due to Persulfate Salts*: Diagnosis and Follow-up FREE TO VIEW

Xavier Muñoz; María-Jesús Cruz; Ramon Orriols; Carlos Bravo; Meritxell Espuga; Ferran Morell
Author and Funding Information

*From the Servei de Pneumología, Hospital Universitari Vall d’Hebron, Barcelona, Spain.

Correspondence to: Xavier Muñoz, Servei de Pneumologia, Hospital General Vall d’Hebron, Passeig Vall d’Hebron, 119, 08035 Barcelona, Spain; e-mail: xmunoz@vhebron.net.es



Chest. 2003;123(6):2124-2129. doi:10.1378/chest.123.6.2124
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Published online

Background: Persulfate salts have been identified as a cause of occupational asthma (OA). The aim of the present study was to describe the clinical characteristics, diagnostic testing results, and follow-up of eight patients with OA that was triggered by these chemical compounds.

Methods: Eight patients with OA due to exposure to persulfate salts were studied. Immunologic, lung function, and specific bronchial challenge tests (SBCTs) were performed in all patients. Once their condition had been diagnosed, the patients were seen every 1, 3, and 6 months for a mean duration of 18 months.

Results: The mean time of exposure to persulfate salts up to diagnosis was 15 years (range, 3 to 27 years), and mean time that had elapsed between symptom onset and diagnosis was 38 months (range, 3 to 120 months). Three patients were smokers, six patients presented with rhinitis prior to asthma in relation to persulfate exposure, and three presented with dermatitis. The results of total IgE tests were positive in six patients, and the results of skin-prick tests for detection of persulfate salts were positive in five of these patients. The results of a SBCT was positive in the seven patients in whom it was performed. Symptoms persisted in all but one patient and required medical treatment.

Conclusions: The results suggest that the reliable diagnosis of OA due to persulfate salts must be based on the specific challenge test until further experience has been acquired. Despite avoiding exposure, patients continued with symptoms and required treatment for the control of symptoms. Finally, a dependent IgE mechanism appears to be implicated in the pathogenesis of OA due to exposure to persulfate salts.

Figures in this Article

Persulfate salts are highly reactive, low-molecular-weight, chemical compounds that are widely used in different manufacturing processes in the chemical, pharmaceutical, metallurgic, textile, photographic, food, and, particularly, cosmetic industries.1 Although the first cases of occupational asthma (OA) due to persulfate salts were described in hairdressers24 and persulfate production workers in the chemical industry5 30 years ago, the prevalence of the disease remains unknown. Blainey et al6 in a cross-sectional study of employees in a hairdressing salon found that 4 of 23 had OA due to exposure to persulfate salts, and Leino et at7 reported an 0.8% prevalence in Finnish hairdressers. Discrepancies as to incidence also were observed. In this respect, based on the English Registry of Surveillance of Work-related and Occupational Respiratory Disease, Cullinan and Newman Taylor8 estimated the incidence of OA in hairdressers to be around 81 cases per million persons exposed per year, whereas Albin et al9 found an incidence of 3.9 per 1,000 persons exposed per year in female Swedish hairdressers.

Thus, although persulfate-induced asthma may represent up to 4% of all OA cases,10 the mechanism by which persulfate salts induce asthma, the risk factors for its development, the value of diagnostic tests, and the evolution of these patients remain unknown. This may be due to the small number of cases studied systematically. Although several case reports1117 of OA caused by persulfate salts have been published, only two series,6,18 using four and five patients, respectively, have been studied to date. For these very same reasons, the follow-up of these patients is also unknown.

The present report describes the clinical features of, the diagnostic tests conducted in, and the follow-up of the largest series of patients with OA due to this chemical compound that have been published to date.

Study Population

Eight women (mean age, 35 years; range, 23 to 46 years), the total number of patients in whom asthma due to persulfate salts had been diagnosed at our occupational respiratory disease unit between 1997 and 2001, were prospectively studied. Three patients were employed in a cosmetic product factory where they mixed persulfate salts with other chemical agents to produce hair bleaches. Five patients worked with dyes in hairdressing salons. In the latter cases, the hair bleaches containing persulfate salts were supplied to the salon in powder form and the workers mixed them with hydrogen peroxide to form a paste, which then was applied to the hair.

At the time of diagnosis, a clinical history including exhaustive occupational history was taken, and lung function, immunologic, and specific bronchial challenge tests (SBCTs) were performed in all patients.

Lung Function Tests

Spirometry was performed (Datospir 200; Sibel; Barcelona, Spain) according to European Respiratory Society guidelines.19 The reference values used were those proposed by Roca et al20 for the Mediterranean population. Bronchial challenge with methacholine was undertaken using the method described by Chai et al.21 Briefly, a dosimeter (Mefar MB3, Ele H2O; Medicalli; Brescia, Italy) was used, and increasing doses of methacholine (range, 0.003 to 16 mg/mL) were inhaled at 3-min intervals until FEV1 had fallen by 20% of its baseline value or the subject had inhaled the maximum concentration of methacholine. The provocative concentration of a substance (methacholine) causing a 20% fall in FEV1 (PC20) was expressed in milligrams per milliliter. The result of the methacholine challenge was considered to be negative if the PC20 was > 8 mg/mL, according to European Respiratory Society guidelines.22

Subjects were provided with portable peak flow recorders (mini Wright; Clement Clarke International; Harlow, Essex, UK) and diary cards, and were instructed in their use following the indications of Moscato et al.23 They were requested to record peak expiratory flow (PEF) rates at least four times per day for 2 weeks at work and 2 weeks off work. The recording was considered to be positive when the qualitative assessment made by one of the authors, an expert in this type of reading, revealed evident changes between the exposure periods.24

Immunologic Test

Skin-prick tests to detect common inhalant allergens were performed according to the method described by Pepys.25 A skin-prick test with potassium and ammonium persulfate (Sigma-Aldrich Corporation; St. Louis, MO) also was performed in all subjects. This test was carried out using freshly produced 5% (weight/volume) ammonium and potassium persulfate solutions. A phosphate-buffered saline (PBS) solution was used as a solvent owing to the acidity of the aqueous solutions. Histamine served as a positive control, and a PBS solution served as a negative control. The results of the test were read at 15 min, and were considered to be positive when the largest and smallest diameter of the wheal divided by 2 was ≥ 3 mm greater than that obtained with the negative control (ie, PBS solution). The histamine positive control was > 3 mm in all patients.26

The total IgE level also was measured (UniCAP System; Pharmacia AB; Uppsala, Sweden), and a level > 150 IU/mL was considered to be high.

SBCT

SBCTs with potassium persulfate were performed following the method proposed by Pepys and Hutchcroft27 for chemical agents and the European Respiratory Society guidelines.22 Subjects were admitted to the hospital for the duration of the test. On the first day, 5 g potassium persulfate were mixed with 150 g lactose and were tipped from one tray into another 30 cm away in a challenge room with independent air extraction. On successive days, if the test proved negative, then 10, 15, and 30 g potassium persulfate mixed with 150 g lactose were tested. All subjects were challenged for 10 min, unless respiratory symptoms developed before that time, in which case the challenge was stopped. Changes in pulmonary function were followed in all patients by measuring FEV1 and FVC at 10-min intervals for the first hour and at hourly intervals thereafter. A response was considered to be positive when FEV1 fell by > 20% of its baseline value in the absence of any change in response to a control challenge of lactose powder alone that was conducted on a separate day.

Follow-up

All patients were advised to avoid exposure to persulfate salts. Medical appointments with forced spirometry were held at 1 month, 3 months, and, later, every 6 months postdiagnosis. Inhaled bronchodilators and/or corticosteroids (depending on the patient’s symptoms, physical examination, and spirometry results) were administered according to the criteria proposed by the Global Initiative for Asthma.28

Clinical Characteristics

Clinical characteristics of the patients are shown in Table 1 . The mean time of contact with persulfate salts prior to diagnosis was 15 years (range, 3 to 27 years), and the mean time elapsed between symptom onset and diagnosis was 38 months (range, 3 to 120 months). All patients developed cough, chest tightness, and wheezing, and initially presented symptoms after work and at night, except patient 7 whose symptoms had occurred during work from the beginning of onset. Symptoms later worsened, appearing also during the day and with no improvement in exposure-free periods, except in patient 6. Three patients (2, 4, and 5) had to attend the emergency department on some occasion, although only patient 2 required hospital admission. Three patients were smokers. Six patients presented with rhinitis prior to their asthma that was related to contact with persulfate salts, and three patients presented with dermatitis. No patient had experienced asthma, rhinitis, or dermatitis prior to initiating contact with persulfate salts.

Lung Function Tests

The results of spirometry and methacholine tests are detailed in Table 2 . All patients had normal spirometry findings at the time of diagnosis. The methacholine test was positive in all patients except one (patient 4).

PEF monitoring was consistent with OA in all cases in which it was performed, with the exception of patient 8. This study was not conducted in patients 1 and 4 as they had left their work during the diagnostic study period.

Immunologic Test

A skin-prick test to detect exposure to persulfate salts was positive in five patients, as shown in Table 2 . Patient 6 presented with an anaphylactic reaction when the prick test to persulfates was performed, with severe bronchospasm that resolved with the administration of topical bronchodilators, subcutaneous adrenaline, and systemic corticosteroids.

Skin-prick tests against potassium and ammonium persulfate also were performed in three healthy subjects and three nonexposed asthmatic patients who served as control subjects. The tests were negative in all of these patients. Total IgE values proved to be high in six patients.

SBCT

SBCT was positive in the seven patients in whom it was performed, eliciting an early response in one patient, a late response in five patients, and a dual response in one patient (Fig 1 and Table 2 ).

Patient 6 did not undergo the SBCT since, as mentioned previously, she presented with severe bronchospasm when the skin-prick test for detecting exposure persulfate salts was performed. The test also was performed in three healthy subjects and three asthmatic subjects, and the findings were negative in all.

Follow-up

The mean duration of follow-up was 18 months (range, 6 to 36 months). The clinical evolution and FEV1 of each patient are detailed in Table 3 . Five patients avoided exposure to persulfate salts, and three patients adopted protective measures following diagnosis. Except for one patient (patient 3), all continued with asthma symptoms and required medical treatment for control of those symptoms. Furthermore, a deterioration in FEV1 was observed in five patients despite the medical treatment.

From the small proportion of exposed workers who develop OA due to persulfate salts,68 the latent period between onset of exposure and the onset of symptoms, and the type of response observed in the challenge test suggest that persulfate-induced OA is mediated by an immunologic mechanism. The results obtained in the present study suggest that this immunologic mechanism might be mediated by IgE, since a skin-prick test that is positive for persulfate salts had been obtained in five patients (62%), as also has been observed in approximately 50% of the cases that have been published to date.34,6,8,11 Furthermore, elevated serum total IgE levels were observed in six patients, and one patient experienced an anaphylactic reaction. Both events also have been described by other authors.13,12,14 However, other mechanisms also may be involved. Blainey et al6 suggested that mast cells may play a role in the pathogenesis of the late asthmatic reactions following the inhalation of persulfate salts, since they found a significant rise in serum neutrophil chemotactic activity paralleling airflow obstruction. Finally, Yawalkar et al1 suggested that T cells may play a role in the pathogenesis of OA due to persulfate salts after reporting a case in which skin-prick test positivity was observed after 24 h and histologic examination of the patient’s late reaction demonstrated a perivascular infiltration predominantly comprising T lymphocytes. This late response to the skin test was not observed in any of our patients.

The diagnosis of OA is usually suggested by clinical history; however, it is often not sufficient to reach a definitive diagnosis29 and should be complemented by serial measurements of PEF, immunologic testing, and/or bronchial challenge testing. Immunologic tests are of little use for the diagnosis of persulfate-induced OA since the sensitivity and specificity of the skin-prick test, which in our series was positive in five of eight patients, remain unknown. In this respect, a 1995 study13 showed that 8 of 52 subjects who had been exposed to persulfate salts had positive skin-prick tests, regardless of whether they had experienced respiratory symptoms or not. On the other hand, in the different works published in which a specific IgE to persulfate salts was studied, no positive values could be found. In our experience, the PEF study proved useful since a response that was consistent with OA was elicited in all but one of the patients in whom it could be performed. Conversely, in the series of Blainey et al,6 only one of four patients showed a consistent response, and Anconetani et al17 published a case in which the PEF study was also negative.

Bearing in mind that the main exposure to persulfate salts occurs in hairdressers, who also may be exposed to other agents (such as henna30 or paraphenylenediamine31 ) that also can cause OA, or to different nonspecific irritants that are capable of triggering bronchospasms in individuals with or without asthma,32 the performance of specific challenge tests for persulfate salts may be indicated in many patients. Different methods of performing this test have been used. Some authors have carried out the test by attempting to reproduce the conditions in the workplace,45 others by aerosolizing a potassium persulfate nondialyzed extract by a nebulizer.11 Finally, Blainey et al6 performed the test by mixing 30 g bleach powder with 50 g lactose and tipping it from one tray to another 30 cm away in a challenge chamber with independent air extraction. In the latter study, three patients also were challenged with persulfate salts; however, the authors did not detail the characteristics of the mixture. In the present study, the test was performed on consecutive days with the quantity of potassium persulfate increased and mixed with lactose with the following two objectives: to avoid overexposure in potentially sensitive patients; and to attempt to show a possible dose-response relationship, which was observed in patients 1, 2, and 4 of our series (Fig 1) . Late response was the most frequently observed form both in our patients and in those in the literature,,4,6,1112 although three cases of early responses4,15,17 and one of dual response16 also have been reported.

With regard to the evolution of patients in whom asthma due to persulfate salts has been diagnosed and in contrast to the cases described by Macchioni et al,18 we observed that seven of our patients had persistent asthma despite avoiding exposure. It is known that a significant number of patients with OA with latency do not recover, even after several years away from exposure.33 In the case of OA due to exposure to isocyanates, our group34 has shown that approximately 71% of patients continue with bronchial hyperreactivity despite avoiding exposure, a percentage that is similar to that already demonstrated by other authors.35 Similarly, in the case of patients with OA due to western red cedar, approximately 60% of patients who avoid exposure continue to have asthma and require treatment for its control.36 The duration of symptoms before removal from exposure is a prognostic indicator, irrespective of the agent. Early removal from exposure increases the likelihood of recovery.33 In the present series of patients, the latency time between the onset of symptoms and diagnosis was prolonged, ranging from 3 to 120 months, which could account for the unfavorable evolution observed later. Furthermore, worsening in FEV1 was found in two patients who failed to avoid exposure (patients 6 and 7). In this respect, a follow-up study of 280 patients with asthma due to western red cedar exposure showed the longitudinal decline in FEV1 to be significantly greater in those who were still exposed to red cedar compared to those who had been exposed but did not have asthma.,37

In conclusion, the results of the present study suggest that a dependent IgE mechanism is involved in persulfate-induced asthma. Furthermore, they support the theory that early diagnosis and prompt removal from exposure are essential for the treatment of these patients, as generally occurs in all patients with OA. Finally, until other tests provide more diagnostic precision, the diagnosis of OA due to persulfate salts must be based in many cases on the specific challenge test.

Abbreviations: OA = occupational asthma; PBS = phosphate-buffered saline; PC20 = provocative concentration of a substance causing a 20% fall in FEV1; PEF = peak expiratory flow; SBCT = specific bronchial challenge test

Table Graphic Jump Location
Table 1. Clinical Characteristics of Patients Studied
* 

In relation to contact with persulfate salts.

Table Graphic Jump Location
Table 2. Results of Diagnostic Tests Performed in the Patients Studied*
* 

+ = positive; − = negative; ND = not done.

 

Ammonium/potassium.

 

Severe bronchospasm after skin-prick test with persulfates.

Figure Jump LinkFigure 1. Bronchial response to SBCT with potassium persulfate in the study population.Grahic Jump Location
Table Graphic Jump Location
Table 3. Follow-up Details Obtained in Eight Patients*
* 

Latest control-FEV1 data obtained at the last appointment of the patients with the physician in the outpatients’ department, prior to the writing of the manuscript.

 

Values in parentheses refer to the classification of patients according to the Global Initiative for Asthma.

The authors are grateful to Christine O’Hara for her help with the English translation of the article, to Teresa Codinach, a member of the nursing staff, and to Rosa Lloria for editorial assistance.

Yawalkar, N, Helbling, A, Pichler, CE, et al (1999) T cell involvement in persulphate triggered occupational contact dermatitis and asthma.Ann Allergy Asthma Immunol82,401-404. [PubMed] [CrossRef]
 
Gaultier, M, Gervais, P, Mellerio, F Deux causes d’asthme professionel chez les coiffeurs: persulphate et soie.Arch Mal Prof1966;27,809-813. [PubMed]
 
Fisher, AA, Dooms-Goosens, A Persulphate hair bleach reactions: cutaneous and respiratory manifestations.Arch Dermatol1976;112,1407-1409. [PubMed]
 
Pepys, J, Hutchcroft, BJ, Breslin, ABX Asthma due to inhaled chemical agents-persulphate salts and henna in hairdressers.Clin Allergy1976;6,399-404. [PubMed]
 
Baur, X, Fruhmann, G, Liebe, VV Occupational asthma and dermatitis after exposure to dust of persulphate salts in two industrial workers.Respiration1979;38,144-150. [PubMed]
 
Blainey, AD, Ollier, S, Cundell, D, et al Occupational asthma in a hairdressing salon.Thorax1986;41,42-50. [PubMed]
 
Leino, T, Tammilehto, L, Hytonen, M, et al Occupational skin and respiratory diseases among hairdressers.Scand J Work Environ Health1998;24,398-406. [PubMed]
 
Cullinan, P, Newman Taylor, AJ Aetiology of occupational asthma.Clin Exp Allergy1997;27(suppl),41-46
 
Albin, M, Rylander, L, Mikoczy, Z, et al Incidence of asthma in female Swedish hairdressers.Occup Environ Med2002;59,119-123. [PubMed]
 
Kopferschmitt-Kubler, MC, Ameille, J, Popin, E, et al Occupational asthma in France: a 1-yr report of the Observatoire National de Asthmes Professionnels project.Eur Respir J2002;19,84-89. [PubMed]
 
Parra, FM, Igea, JM, Quirce, S, et al Occupational asthma in a hairdresser caused by persulphate salts.Allergy1992;47,656-660. [PubMed]
 
Gamboa, PM, Cuesta, Gc, Garcia, BE, et al Late asthmatic reaction in a hairdresser, due to the inhalation of ammonium persulphate salts.Allergol Immunopathol (Madr)1989;17,109-111. [PubMed]
 
Wrbitzky, R, Drexler, H, Letzel, S Early reaction type allergies and diseases of the respiratory passages in employees from persulphate production.Int Arch Occup Environ Health1995;67,413-417. [PubMed]
 
Meindl, K, Meyer, R Asthma and urticaria in hairdressers caused by bleaching agents containing persulphates.Zentralbl Arbeitsmed1969;3,75-79
 
Azofra, J, Jarilla, JL Asma ocupacional por persulfatos [abstract]. Rev Esp Alergol Inmunol Clin. 1990;;5(suppl) ,.:145
 
Mira, J, Joral, A, Boynao, T Asma profesional por persulfatos mediada por IgE [abstract]. Rev Esp Alergol Inmunol Clin. 1990;;5(suppl) ,.:81
 
Pablo Anconetani, J, Isabel Badorrey, M, Monsó, E, et al Asma laboral por persulfatos: escasa utilidad diagnóstica de la determinación del flujo expiratorio máximo en el lugar de trabajo [letter]. Med Clin (Barc). 2001;;116 ,.:355. [PubMed]
 
Macchioni, P, Kotopoulos, C, Talini, D, et al Asthma in hairdressers: a report of 5 cases.Med Lav1999;90,776-785. [PubMed]
 
Quanjer, PH, Tammeling, GJ, Cotes, JE, et al Lung volumes and forced ventilatory flows.Eur Respir J1993;6(suppl),5-40
 
Roca, J, Sanchís, J, Agustí-Vidal, A, et al Spirometric reference values from a Mediterranean population.Bull Eur Physiopathol Respir1986;22,217-224. [PubMed]
 
Chai, H, Farr, R, Froehlich, LA, et al Standardization of bronchial inhalation challenge procedures.J Allergy Clin Immunol1975;56,323-327. [PubMed]
 
Sterk, PJ, Fabbri, LM, Quanjer, PhH, et al Airway responsiveness: standardized challenge testing with pharmacological, physical and sensitizing stimuli in adults.Eur Respir J1993;6(suppl),53-83
 
Moscato, G, Godnic-Cvar, J, Maestrelli, P, et al Statement on self-monitoring of peak expiratory flows in the investigation of occupational asthma.Eur Respir J1995;8,1605-1610. [PubMed]
 
Cote, J, Kennedy, S, Chang-Yeung, M Quantitative versus qualitative analysis of peak expiratory flow in occupational asthma.Thorax1993;48,48-51. [PubMed]
 
Pepys, J Skin test in diagnosis. Gell, PGH Coombes, RRA Lachman, PJ eds.Clinical aspects of immunology 3rd ed.1975,55-80 Blackwell Scientific Publications. Oxford, UK:
 
Morell, F, Codina, R, Rodrigo, MJ Increased positivity of skin test and allergenic stability of glycerinated soybean hull extracts.Clin Exp Allergy1999;29,388-393. [PubMed]
 
Pepys, J, Hutchcroft, BJ Bronchial provocation test in aetiology diagnosis and analysis of asthma.Am Rev Respir Dis1975;112,829-859. [PubMed]
 
Global Initiative for Asthma.. Global strategy for asthma management and prevention: NHLBI/WHO workshop report. 1998; National Institutes of Health, National Heart Lung and Blood Institute. Bethesda, MD: NIH Publication No. 96–3659B.
 
Malo, JL, Ghezzo, H, L’Archevêque, J, et al Is the clinical history a satisfactory means of diagnosing occupational asthma?Am Rev Respir Dis1991;143,528-532. [PubMed]
 
Starr, JC, Yunginger, J, Brahser, GW Immediate type I asthmatic response to henna following occupational exposure in hairdressers.Ann Allergy1982;48,98-99. [PubMed]
 
Gelfand, HH Respiratory allergy due to chemical compounds encountered in the rubber, lacquer, shellac, and beauty culture industries.J Allergy1963;34,374-381. [PubMed]
 
Zuskin, E, Bouhuys, A Acute airway responses to hairspray preparations.N Engl J Med1974;290,660-663. [PubMed]
 
Chan-Yeung, M Occupational asthma.Chest1990;98(suppl),148S-161S
 
Orriols, R, Drobnic, ME, Muñoz, X, et al Asma ocupacional por isocianatos: estudio de 21 pacientes.Med Clin (Barc)1999;113,659-662. [PubMed]
 
Mapp, C, Arone, P, Marzo, N, et al Persistent asthma due to isocyanates: a follow-up study of subjects with occupational asthma due to toluene diisocyanate.Am Rev Respir Dis1988;137,1326-1329. [PubMed]
 
Chan-Yeung, M, MacLean, L, Paggiaro, PL Follow-up study of 232 patients with occupational asthma caused by western red cedar (Thuja plicata).J Allergy Clin Immunol1987;79,792-796. [PubMed]
 
Lin, FJ, Dimich-Ward, H, Kennedy, S, et al Longitudinal decline in lung function in patients with occupational asthma due to western red cedar.Occup Environ Med1996;53,753-756. [PubMed]
 

Figures

Figure Jump LinkFigure 1. Bronchial response to SBCT with potassium persulfate in the study population.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Clinical Characteristics of Patients Studied
* 

In relation to contact with persulfate salts.

Table Graphic Jump Location
Table 2. Results of Diagnostic Tests Performed in the Patients Studied*
* 

+ = positive; − = negative; ND = not done.

 

Ammonium/potassium.

 

Severe bronchospasm after skin-prick test with persulfates.

Table Graphic Jump Location
Table 3. Follow-up Details Obtained in Eight Patients*
* 

Latest control-FEV1 data obtained at the last appointment of the patients with the physician in the outpatients’ department, prior to the writing of the manuscript.

 

Values in parentheses refer to the classification of patients according to the Global Initiative for Asthma.

References

Yawalkar, N, Helbling, A, Pichler, CE, et al (1999) T cell involvement in persulphate triggered occupational contact dermatitis and asthma.Ann Allergy Asthma Immunol82,401-404. [PubMed] [CrossRef]
 
Gaultier, M, Gervais, P, Mellerio, F Deux causes d’asthme professionel chez les coiffeurs: persulphate et soie.Arch Mal Prof1966;27,809-813. [PubMed]
 
Fisher, AA, Dooms-Goosens, A Persulphate hair bleach reactions: cutaneous and respiratory manifestations.Arch Dermatol1976;112,1407-1409. [PubMed]
 
Pepys, J, Hutchcroft, BJ, Breslin, ABX Asthma due to inhaled chemical agents-persulphate salts and henna in hairdressers.Clin Allergy1976;6,399-404. [PubMed]
 
Baur, X, Fruhmann, G, Liebe, VV Occupational asthma and dermatitis after exposure to dust of persulphate salts in two industrial workers.Respiration1979;38,144-150. [PubMed]
 
Blainey, AD, Ollier, S, Cundell, D, et al Occupational asthma in a hairdressing salon.Thorax1986;41,42-50. [PubMed]
 
Leino, T, Tammilehto, L, Hytonen, M, et al Occupational skin and respiratory diseases among hairdressers.Scand J Work Environ Health1998;24,398-406. [PubMed]
 
Cullinan, P, Newman Taylor, AJ Aetiology of occupational asthma.Clin Exp Allergy1997;27(suppl),41-46
 
Albin, M, Rylander, L, Mikoczy, Z, et al Incidence of asthma in female Swedish hairdressers.Occup Environ Med2002;59,119-123. [PubMed]
 
Kopferschmitt-Kubler, MC, Ameille, J, Popin, E, et al Occupational asthma in France: a 1-yr report of the Observatoire National de Asthmes Professionnels project.Eur Respir J2002;19,84-89. [PubMed]
 
Parra, FM, Igea, JM, Quirce, S, et al Occupational asthma in a hairdresser caused by persulphate salts.Allergy1992;47,656-660. [PubMed]
 
Gamboa, PM, Cuesta, Gc, Garcia, BE, et al Late asthmatic reaction in a hairdresser, due to the inhalation of ammonium persulphate salts.Allergol Immunopathol (Madr)1989;17,109-111. [PubMed]
 
Wrbitzky, R, Drexler, H, Letzel, S Early reaction type allergies and diseases of the respiratory passages in employees from persulphate production.Int Arch Occup Environ Health1995;67,413-417. [PubMed]
 
Meindl, K, Meyer, R Asthma and urticaria in hairdressers caused by bleaching agents containing persulphates.Zentralbl Arbeitsmed1969;3,75-79
 
Azofra, J, Jarilla, JL Asma ocupacional por persulfatos [abstract]. Rev Esp Alergol Inmunol Clin. 1990;;5(suppl) ,.:145
 
Mira, J, Joral, A, Boynao, T Asma profesional por persulfatos mediada por IgE [abstract]. Rev Esp Alergol Inmunol Clin. 1990;;5(suppl) ,.:81
 
Pablo Anconetani, J, Isabel Badorrey, M, Monsó, E, et al Asma laboral por persulfatos: escasa utilidad diagnóstica de la determinación del flujo expiratorio máximo en el lugar de trabajo [letter]. Med Clin (Barc). 2001;;116 ,.:355. [PubMed]
 
Macchioni, P, Kotopoulos, C, Talini, D, et al Asthma in hairdressers: a report of 5 cases.Med Lav1999;90,776-785. [PubMed]
 
Quanjer, PH, Tammeling, GJ, Cotes, JE, et al Lung volumes and forced ventilatory flows.Eur Respir J1993;6(suppl),5-40
 
Roca, J, Sanchís, J, Agustí-Vidal, A, et al Spirometric reference values from a Mediterranean population.Bull Eur Physiopathol Respir1986;22,217-224. [PubMed]
 
Chai, H, Farr, R, Froehlich, LA, et al Standardization of bronchial inhalation challenge procedures.J Allergy Clin Immunol1975;56,323-327. [PubMed]
 
Sterk, PJ, Fabbri, LM, Quanjer, PhH, et al Airway responsiveness: standardized challenge testing with pharmacological, physical and sensitizing stimuli in adults.Eur Respir J1993;6(suppl),53-83
 
Moscato, G, Godnic-Cvar, J, Maestrelli, P, et al Statement on self-monitoring of peak expiratory flows in the investigation of occupational asthma.Eur Respir J1995;8,1605-1610. [PubMed]
 
Cote, J, Kennedy, S, Chang-Yeung, M Quantitative versus qualitative analysis of peak expiratory flow in occupational asthma.Thorax1993;48,48-51. [PubMed]
 
Pepys, J Skin test in diagnosis. Gell, PGH Coombes, RRA Lachman, PJ eds.Clinical aspects of immunology 3rd ed.1975,55-80 Blackwell Scientific Publications. Oxford, UK:
 
Morell, F, Codina, R, Rodrigo, MJ Increased positivity of skin test and allergenic stability of glycerinated soybean hull extracts.Clin Exp Allergy1999;29,388-393. [PubMed]
 
Pepys, J, Hutchcroft, BJ Bronchial provocation test in aetiology diagnosis and analysis of asthma.Am Rev Respir Dis1975;112,829-859. [PubMed]
 
Global Initiative for Asthma.. Global strategy for asthma management and prevention: NHLBI/WHO workshop report. 1998; National Institutes of Health, National Heart Lung and Blood Institute. Bethesda, MD: NIH Publication No. 96–3659B.
 
Malo, JL, Ghezzo, H, L’Archevêque, J, et al Is the clinical history a satisfactory means of diagnosing occupational asthma?Am Rev Respir Dis1991;143,528-532. [PubMed]
 
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