Jörn Nielsen

Incidence of asthma in female Swedish hairdressers

Objective: To investigate the risk of asthma in hairdressers. Methods: The incidence of asthma was retrospectively estimated in a Swedish nationwide study including all female hairdressers certified from vocational schools from 1970 to 1995, and a stratified sample of women from the general population were referents. A postal questionnaire included questions on respiratory tract symptoms, atopy, smoking, working periods as a hairdresser, and number of specific hair treatments performed/week. Reported exposures were validated by occupational hygienists. Rate ratios of incidence (IRRs) of asthma were estimated by Poisson regression, adjusted for calendar year of observation, hay fever, smoking, and region of domicile. Results: The crude incidences of asthma/1000 person-years were: 3.9 during active years as a hairdresser, 2.8 among the hairdressers when not working in the profession, and 3.1 among the referents. The corresponding IRR for being an active hairdresser compared with the referents was 1.3 (95% confidence interval (95% CI) 1.0 to 1.6). Moderate effects on risk of asthma were found both from hairdressing work (IRR=1.6 (1.1 to 2.2) among never-smokers) and from smoking (IRR=1.6 (1.2 to 2.2) among referents). However, the combined effect from hairdressing work and smoking (IRR=1.5 (1.0 to 2.1)) was less than expected (p=0.02). No effect modification by respiratory atopy was found. The hairdressers most often performing hair bleaching treatments (IRR=1.5 (0.7 to 3.0)) or using hair spray (IRR=1.4 (0.8 to 2.4)) had, compared with the most infrequent users, a slightly, but not significantly higher incidence of asthma. Exposure to persulphates in hair bleach was estimated to be 0.04–0.15 mg/m3 during mixing of the powder. Reported average number of bleaching treatments agreed well with those performed according to a diary. Conclusions: Active hairdressing work was associated with a moderately increased incidence of asthma among lifelong non-smokers. The results are moderately supportive, but not conclusive, of associations between asthma and exposure to hair bleach or hair spray.

Assessment of environmental tobacco smoke exposure in children with asthmatic symptoms by questionnaire and cotinine concentrations in plasma, saliva, and urine

To validate a detailed questionnaire for assessment of environmental tobacco smoke (ETS) exposure by the biomarker cotinine in various media, a population-based study in the urban area of Malmö, Sweden was performed in children aged 8-13 years with and without asthmatic symptoms. There were strong correlations between urinary and saliva cotinine concentrations and also, though to a lesser extent, between these media and plasma. Even a detailed questionnaire gave only a rough picture of the ETS exposure, as indicated by the biomarkers. In a multivariate model, the most significant questionnaire-derived predictor of the cotinine levels was the maternal smoking habits; other questionnaire variables gave only a minimal explained variance. Children with a history of asthmatic symptoms had statistically significantly lower median cotinine levels in urine and saliva compared to referent children, most likely because of the antismoking information to their parents. This should be considered in epidemiological studies of ETS risks.

Incidence of hand eczema in female Swedish hairdressers

Objective: To estimate the occurrence of hand eczema in hairdressers in Sweden. Methods: The occurrence of hand eczema was estimated in a Swedish longitudinal retrospective cohort study including all female graduates from vocational schools for hairdressers from 1970 to 1995. A stratified sample from the general population acted as controls. A self-administered questionnaire including questions on the occurrence of hand eczema, skin atopy, working periods and number of hair treatments performed per week was sent to the participants. Incidence rate ratios (IRRs) of hand eczema were estimated. Results: The incidence rate of hand eczema in hairdressers was 23.8 cases/1000 person-years, whereas in hairdressers who were aged <25 years it was 37.1/1000 person-years. The corresponding IRR for hairdressers compared with controls was 2.5 (95% confidence interval (CI) 2.2 to 2.8), and that for younger hairdressers was 3.1 (95% CI 2.6 to 3.5). The mean age at onset of hand eczema was 21.6 years for hairdressers and 21.2 years for controls. The 1-year prevalence of hand eczema was 18.0% for hairdressers and 12.1% for controls. A large number of hair treatments involving exposure to skin irritants and sensitisers were reported. The incidence rate of hand eczema was higher among individuals with a history of childhood eczema, both for hairdressers and for controls, giving an (age-adjusted) IRR of 1.9 and 2.2, respectively. The attributable fraction of hand eczema from skin atopy was 9.6%. A synergistic effect of skin atopy and hairdressing was found on the occurrence of hand eczema. The relative excess risk due to interaction was 1.21 (95% CI 0.21 to 2.21; p = 0.01). Conclusion: Hairdressers are highly exposed to skin-damaging substances. The self-reported incidence of hand eczema was substantially higher in female hairdressers than in controls from the general population and than that found previously in register-based studies. For many individuals, onset of hand eczema occurs early in life. Only about 10% of the hand eczema cases among hairdressers would be prevented if no one with skin atopy entered the trade.

Specific antibodies to methyltetrahydrophthalic anhydride in exposed workers

A group of 145 workers exposed to methyltetrahydrophthalic anhydride (MTHPA) was investigated. They were working in a plant which, since 1983, handled an epoxy resin with MTHPA as a hardener. Specific IgE antibodies (RAST) to a conjugate between MTHPA and human serum albumin (HSA) were statistically significantly increased (P= 0·001; 26 subjects = 18% positive) in the exposed group, compared to a non‐exposed control group (n= 33). One positive worker was only exposed for 2 months. Twenty‐three exposed subjects were also skin‐prick test positive to MTHPA‐HSA. The exposed group was divided into three different exposure categories, according to their contact with the epoxy resin. The average exposure levels at the time of the investigation were, in zone 10·085 mg/m3, in zone II0·014 mg/m3, and in zone III 0·010 mg/m3, though the exposure probably had been higher earlier. There was an association between exposure intensity and RAST‐positive persons (P= 0·0025, chi‐square trend test). Forty‐four persons (30%) were smokers, and 16(11%) atopics. No association between sensitization and either atopy or smoking was found. There was an association between exposure intensity and specific IgG antibodies (P= 0·0003, chi‐square trend test). Specific IgG4 antibodies were closely related to specific total IgG antibodies (P= 0·0001). These findings demonstrate that MTHPA is a sensitizing agent at low levels of exposure.

Allergy to methyltetrahydrophthalic anhydride in epoxy resin workers.

One hundred and forty four current and 26 former workers in a plant producing barrels for rocket guns from an epoxy resin containing methyltetrahydrophthalic anhydride (MTHPA; time weighted average air concentration up to 150 micrograms/m3) were studied. They showed higher frequencies of work related symptoms from the eyes (31 v 0%; p < 0.001), nose (53 v 9%; p < 0.001), pharynx (26 v 6%; p < 0.01), and asthma (11 v 0%; p < 0.05) than 33 controls. Also they had higher rates of positive skin prick test to a conjugate of MTHPA and human serum albumin (16 v 0%; p < 0.01), and more had specific IgE and IgG serum antibodies (18 v 0%; p < 0.01 and 12 v 0%; p < 0.05 respectively). There were statistically significant exposure-response relations between exposure and symptoms from eyes and upper airways, dry cough, positive skin prick test, and specific IgE and IgG antibodies. There was a non-significant difference in reaction to metacholine between exposed workers and non-smoking controls. In workers with and without specific IgE antibodies, differences existed in frequency of nasal secretion (54 v 23%; p < 0.05) and dry cough (38 v 12%; p < 0.05). Workers with specific IgG had more dry cough (38 v 12%; p < 0.05), but less symptoms of non-specific bronchial hyperreactivity (0 v 26%; p < 0.05). Atopic workers sneezed more than non-atopic workers (65 v 30%; p < 0.01). In a prospective study five sensitised workers who left the factory became less reactive to metacholine, and became symptom free. In 41 workers who stayed, there was no improvement, despite a 10-fold reduction in exposure. The results show the extreme sensitising properties of MTHPA.

Effects of diesel exposure on lung function and inflammation biomarkers from airway and peripheral blood of healthy volunteers in a chamber study.

BackgroundExposure to diesel exhaust causes inflammatory responses. Previous controlled exposure studies at a concentration of 300 μg/m3 of diesel exhaust particles mainly lasted for 1 h. We prolonged the exposure period and investigated how quickly diesel exhaust can induce respiratory and systemic effects.MethodsEighteen healthy volunteers were exposed twice to diluted diesel exhaust (PM1 ~300 μg/m3) and twice to filtered air (PM1 ~2 μg/m3) for 3 h, seated, in a chamber with a double-blind set-up. Immediately before and after exposure, we performed a medical examination, spirometry, rhinometry, nasal lavage and blood sampling. Nasal lavage and blood samples were collected again 20 h post-exposure. Symptom scores and peak expiratory flow (PEF) were assessed before exposure, and at 15, 75, and 135 min of exposure.ResultsSelf-rated throat irritation was higher during diesel exhaust than filtered air exposure. Clinical signs of irritation in the upper airways were also significantly more common after diesel exhaust exposure (odds ratio=3.2, p<0.01). PEF increased during filtered air, but decreased during diesel exhaust exposure, with a statistically significant difference at 75 min (+4 L/min vs. -10 L/min, p=0.005). Monocyte and total leukocyte counts in peripheral blood were higher after exposure to diesel exhaust than filtered air 20 h post-exposure, and a trend (p=0.07) towards increased serum IL-6 concentrations was also observed 20 h post-exposure.ConclusionsDiesel exhaust induced acute adverse effects such as symptoms and signs of irritation, decreased PEF, inflammatory markers in healthy volunteers. The effects were first seen at 75 min of exposure.

IgG antibodies against polyisocyanates in car painters

A group of thirty car painters exposed to vapours and aerosols of paint containing prepolymer and monomer of hexametylene diisocyanate (HDI) was investigated. Specific antibodies against monomer HDI and prepolymerized HDI were analysed with RAST (IgE) and ELISA (IgG) assays after conjugation of the haptens with human serum albumin. There was no significant increase of serum IgG antibodies against HDI monomer, nor of specific IgE antibodies against HDI monomer or prepolymer. Specific IgG antibodies against prepolymerized HDI were significantly increased, as compared with non‐exposed referents (medians 0.11 vs 0.03 absorbance (A)). Six car painters were found to have specific IgG antibodies of subclass 4 against HDI prepolymer, four also against HDI monomer. This shows an association between exposure and specific IgG antibodies. Thirteen subjects had suffered symptoms of rhinitis and/or conjunctivitis, and ten had symptoms from the bronchi (two asthma). There was no significant association between symptoms and levels of specific antibodies. Most of the symptoms were slight and unspecific, probably due to irritative effects of the exposure.

Nasal challenge shows pathogenetic relevance of specific IgE serum antibodies for nasal symptoms caused by hexahydrophthalic anhydride

Abstract. Hexahydrophthalic anhydride (HHPA) is a component of some epoxy resin systems, A high fraction of HHPA‐exposed workers display nasal symptoms, and some of them have specific serum antibodies. To test the pathogenetic relevance of the antibodies, nasal challenge tests were performed with a conjugate of HHPA and human serum albumin (HSA) at three increasing concentrations. Eleven subjects, who were IgE‐sensitized against HHPA (positive in RAST and in skin‐prick test against the HHPA‐HSA conjugate), and who reported work‐related nasal symptoms, had a significant increase of nasal symptoms and a decrease of nasal inspiratory peak flow after the challenges. The symptoms were associated with specific serum IgE, but with IgG. Further, significant increases were found in eosinophil and neutrophil counts, and in levels of tryptase, and albumin, whereas no clear rise was recorded for eosinophil cationic protein in nasal lavage fluid. Nine subjects, who were not sensitized, but who complained of work‐related nasal symptoms, and 11 subjects, who were not sensitized and had no symptoms, displayed no significant change in any of these parameters. It is concluded that the symptoms in some of the workers were caused by an IgE‐mediated mast cell degranulation. followed by an inflammatory reaction, engaging eosinophil and neutrophil cells.

Association of HLA‐DQ5 and HLA‐DR1 with sensitization to organic acidanhydrides

Background Organic acid anhydrides are low molecular weight industrial chemicals, able to cause rhinoconjunctivitis and asthma associated with specific IgE against hapten–carrier protein conjugate. Only a proportion of exposed workers develop IgE‐associated allergy to acid anhydrides.

Immunologic tests of specific antibodies to organic acid anhydrides

The outcome of immunologic tests of antibodies directed against hapten conjugates of organic acid anhydrides and human serum albumin (HSA) has been studied in workers exposed to phthalic anhydride (PA), methyltetrahydroplithalic anhydride (MTHPA), hexahydrophthalic anhydride (HHPA), and methylhexahydrophthalie anhydride (MHHPA). HSA conjugates of PA, MTHPA, HHPA, MHHPA, and nialeic anhydride (MA) have been prepared and used in the tests. The hapten densities (HD) of the conjugates were varied by different molar ratios of hapten and macromolecule in the preparative procedure. Skin prick reactions to MTHPA‐HSA increased with rising HD over the range 6‐13 mol/mol. The achieved HD was tested by spectrometric and gas chromatographic methods. In RAST of IgE antibodies MTHPA‐HSA with HD six and 25 showed significantly lower bindings than conjugates with intermediate HD. There was a good correlation between skin prick tests and RAST. Of 234 workers tested [MTHPA (n= 145), and HHPA (n= 89)], 45 had a skin prick reaction > 50% of the histamine reaction (1 mg/ml). All but two of these were RAST positive (RAST value > 0.3%; 0.3% upper range in 147 controls; MTHPA, n= 63; HHPA, n= 84). Nine RAST positive workers had no obvious skin prick reaction. However, their RAST values were low (<0.8%). In exposed workers, the ELISA value of specific IgG antibodies to MTHPA‐HSA showed optimal values when tested with the HD 13 conjugate. The specific antibodies in workers exposed to either MTHPA or HHPA/MHHPA showed a marked cross‐reactivity to MTHPA‐HSA, HHPA‐HSA, and MHHPA‐HSA as proven by skin prick tests, RAST, and RAST inhibition. In workers exposed lo PA (here was less cross reactivity to the other anhydrides.