Bronchial reactivity after provocation of the nasal mucosa with histamine]

Data on the relationship between nasal and bronchial reactivities are scarce. This study aimed at investigating a possible influence of the nasal provocation test on bronchial reactivity. Three groups of eleven subjects each were examined: patients suffering from allergic rhinitis with no clinical evidence of asthma, workers exposed to respiratory irritants complaining of occupational rhinitis and asthma, and healthy subjects. Non-specific bronchoprovocation was performed before and after nasal challenge with histamine. The bronchial challenge with histamine solutions (0.125 mg/ml and 128 mg/ml) was performed by the five-breath cumulative method (Chai H. et al. J Allergy Clin Immunol 1975;56:323-7). Non-specific nasal provocation was performed by spraying doubling concentrations of histamine (0.125 mg/ml-32 mg/ml) into both nostrils at three-minute intervals. The reaction was monitored by measurement of nasal inspiratory peak flow, nasal resistance, and nasal spirometry. The level of non-specific nasal reactivity was significantly lower in patients with allergic rhinitis than in the other two groups. The bronchial reactivity of the "rhinitis" group and of those occupationally exposed to irritants was significantly lower than among healthy subjects. An immediate and significant decrease in bronchial reactivity could be observed after nasal challenge in the group of healthy subjects as well as in workers exposed to irritants, but there was no significant change in bronchial reactivity among patients suffering from allergic rhinitis.     

Non-specific nasal and bronchial reactivity are not correlated in non-asthmatic subjects occupationally exposed to irritants and in healthy subjects

BACKGROUND: Non-specific nasal and bronchial reactivity are frequently correlated in disease (rhinitis and asthma). It is not known whether such a correlation exists in subjects exposed to irritants and in healthy subjects. In order to test the hypothesis that a correlation between non-specific nasal and bronchial reactivity exists in non-asthmatic subjects, two groups of subjects were studied: 110 workers occupationally exposed to respiratory irritants, and 86 non-exposed healthy controls. METHODS: Allergy, non-specific nasal, and non-specific bronchial reactivity were tested, and smoking habits were categorized in each subject. RESULTS: Respiratory irritants cause a substantial increase in nasal and bronchial reactivity when compared with the group of healthy, non-exposed subjects (33.6% nasal hyperreactors and 20.0% bronchial hyperreactors vs. 4.7% nasal hyperreactors and 2.3% bronchial hyperreactors, respectively). But, occupational exposure to respiratory irritants does not induce a correlation between non-specific nasal and bronchial reactivity frequently found in asthmatic and rhinitic subjects. CONCLUSIONS: We found no correlation between non-specific nasal and bronchial reactivity either in subjects occupationally exposed to respiratory irritants or in the group of healthy subjects. This lack of correlation in both studied groups seems to be a feature of non-diseased airways. Smoking as an additional factor does not increase nasal and bronchial reactivity either in workers exposed to irritants or in healthy subjects. Smoking also does not strengthen the correlation between upper and lower airways' reactivity in both groups.     

Nonspecific nasal responsiveness in workers occupationally exposed to respiratory irritants

The aim of the study was to establish the level of the nonspecific nasal responsiveness in a group of workers (N = 84) occupationally exposed to respiratory irritants, and to compare it with its level in healthy subjects (N = 60). Another goal was to study the effect of occupational exposure to irritants, smoking, and atopy on nonspecific nasal responsiveness. The modified method of nonspecific nasal provocation with histamine developed by van Wijk and Dieges (Clin Allerg 17:563–570, 1987) was used. The method was performed by spraying doubling concentrations of histamine (0.03–32 mg/mL), starting with saline, in a cumulative manner into each nostril. The reaction was measured by total nasal resistance (“opening” interruption technique). The result of the test was expressed as provocation concentration of histamine that caused ?75% rise of total nasal resistance compared to its value measured after saline. We found a significantly higher percentage of nasal hyperreactors and a significantly greater nonspecific nasal responsiveness among 65 exposed workers (χ² = 78.6; p < 0.001, t = ?5.48; p < 0.001, respectively) than in the group of healthy subjects. A significantly (t = 4.25; p < 0.001) increased nonspecific nasal responsiveness was observed during exposure when compared to nonspecific nasal responsiveness assessed after 2 weeks out of exposure, when tested in 19 patients. Higher smoking rate as measured by smoking category (number of cigarettes multiplied with years of smoking) was associated with the lower levels of nonspecific nasal responsiveness. Also, we failed to confirm a relation between atopy and nonspecific nasal responsiveness in a group of workers exposed to irritants. © 1993 Wiley-Liss, Inc.     

Increase in airway hyperresponsiveness among workers exposed to methylene diphenyldiisocyanate compared to workers exposed to toluene diisocyanate at a petrochemical plant in Korea

BACKGROUND: The purpose of this study was to investigate the prevalence of airway hyperresponsiveness induced by methylene diphenyldiisocyanate (MDI) and toluene diisocyanate (TDI) at a petrochemical industry complex in Korea. METHODS: Questionnaires, allergic skin test, and nonspecific airway hyperresponsiveness (AHR) were studied in 64 exposed workers and 27 control subjects. Questionnaires included questions about symptoms of cough, wheezing, chest tightness, dyspnea, rhinorrhea, sneezing, itching, stuffiness, tearing, urticaria, sore throat, and exacerbating time. Methacholine challenge tests were done. Bronchial responsiveness (BRindex) defined as log (% fall in FEV(1))/log (last concentration of methacholine +10). RESULTS: Prevalence of AHR (PC20 FEV(1) < 16.0 mg/mL of methacholine) was higher in MDI-exposed workers than in TDI-exposed workers [4/20 (20%) vs. 2/42 (4.7%), P<0.05]. Twenty-three workers (36%) of all subjects had respiratory symptoms. MDI-exposed workers, in comparison with control subjects, had higher BRindex (0.73+/-0.04 vs. 0.62+/-0.02, P<0.05). Workers exposed to TDI or MDI who had respiratory symptoms (n = 23), in comparison to workers exposed to TDI or MDI without respiratory symptoms (n = 41), had significantly higher BRindex (0.82+/-0.06 vs. 0.60+/-0.02, P<0.05). FEV(1) was significantly negatively correlated with BRindex (r = -0.253, P<0.05). BRindex was not correlated with atopy, smoking status, and exposure duration. CONCLUSIONS: These findings suggest that workers exposed to MDI are at a higher risk of asthma in comparison with TDI-exposed workers and control subjects at a petrochemical plant in Korea.     

Bronchial reactivity during continuous and interrupted exposure to respiratory irritants

Evolution of bronchial reactivity was examined in a sample of aluminium potroom workers exposed to a variety of respiratory irritants in concentrations below the MAC values for Yugoslavia (hydrogen fluoride, particulate fluorides, sulphur dioxide). Lung function indices and bronchial reactivity were measured in 24 workers continuously employed in an aluminium plant and in nine workers who had ceased to work in the plant. Measurements took place over a two-year interval. A sustained level of bronchial reactivity was recorded in both examined groups regardless of occupational practice. Even in workers with dyspnoea and airway obstruction bronchial reactivity did not worsen in spite of continuous exposure. Avoidance of exposure to potroom fumes did not bring about any significant improvement of reactivity, moreover, bronchial reactivity deteriorated in one worker. Owing to discordance between spirometric values and bronchial reactivity, a follow-up of workers removed from harmful occupational exposure is suggested.     

Reduced epidermal nerve density among hand-transmitted vibration-exposed workers

OBJECTIVE: The objective of this study was to evaluate ultrastructural changes of epidermal nerve density (END) in workers exposed to hand-transmitted vibration. METHODS: Ten male subjects with occupational exposure to hand-transmitted tools for 46.9 hours weekly for an average of 6.5 years were included in this study. We performed a skin biopsy from the forearms and compared the END with 10 age- and gender-matched healthy control subjects. RESULTS: Nine of the 10 subjects had abnormally low END. The END of the exposed workers was significantly lower than the control group (4.1 +/- 2.8 vs 9.0 +/- 4.3 fibers/mm, P = 0.005). The difference remained even after one subject with possible undiagnosed diabetes was not included (4.3 +/- 2.9 vs 9.6 +/- 4.2 fibers/mm, P = 0.005). The reduction of END did not correlate with the abnormality of nerve conduction studies or quantitative sensory testing. CONCLUSIONS: The reduction of END suggested the involvement of small-diameter nerve fibers among this population, and such a histologic change might either be independent or precede changes of large myelinated nerve fibers.     

The respiratory responses of subjects with allergic rhinitis to ozone exposure and their relationship to nonspecific airway reactivity

Ozone exposure in man produces changes in respiratory function and symptoms. There is a large degree of unexplained intersubject variability in the magnitude of these responses. There is concern that individuals with chronic respiratory diseases may also be more responsive to ozone than normal individuals. The purpose of this study was to describe the responses of subjects with allergic rhinitis to ozone exposure and to compare these responses to those previously observed in normal individuals. A further purpose was to measure the association of baseline nonspecific airway reactivity with changes in lung function and respiratory symptoms following ozone exposure. A group of 26 nonasthmatic subjects with allergic rhinitis performed a bronchial inhalation challenge with histamine and subsequently underwent two hour exposures to both clean air and to 0.18 part per million ozone with alternating periods of rest and heavy exercise. The airway reactivity of this group of subjects was no greater than that of a comparable group of subjects without allergic rhinitis. The respiratory responses of these subjects to ozone exposure were similar to those previously reported for subjects without allergic rhinitis with the exception that the allergic rhinitis subjects appeared to have a modestly increased bronchoconstrictor response compared to normals. Furthermore, we observed no significant relationships between nonspecific airway reactivity and response to ozone as measured by changes in lung function or the induction of symptoms.     

Exercise-induced bronchoconstriction in textile and agricultural workers and in bakers

To assess the prevalence and the characteristics of exercise-induced bronchoconstriction (EIB) in subjects occupationally exposed to organic dusts we performed a cross-sectional study including 152 exposed subjects (67 textile workers, 42 agricultural workers, and 43 bakers) and 72 unexposed controls. Evaluation of exposed and unexposed subjects included a questionnaire, skin prick tests to common inhalant allergens, spirometry, and exercise challenge tests (ECT). The EIB prevalence found in textile workers was 8.9 %, in agricultural workers 7.1 %, in bakers 6.9 %, and in office workers 5.5 %. The highest bronchial reaction to exercise was found in ECT-positive agricultural workers (26.1+/-6.9), followed by textile workers (25.2+/-7.4), bakers (23.0+/-5.8), and office workers (21.8+/-4.4). EIB was significantly associated with atopy and positive family history of asthma in all exposed groups. EIB was significantly associated with smoking duration in textile workers (P=0.039) and agricultural workers (P=0.027). Bronchial reaction to exercise was significantly greater in smoking than in non-smoking textile (P=0.045) and agricultural workers (P=0.032). Our data suggest that the combination of daily smoking and workplace exposure to certain types of organic dusts could contribute to EIB development and severity.     

Occupational asthma in subjects occupationally exposed to herbal and fruit tea dust

We performed a cross-sectional study to detect occupational asthma (OA) in 63 subjects occupationally exposed to herbal and fruit tea dust and in 63 corresponding controls. The evaluation included a questionnaire, skin prick tests to workplace and common inhalant allergens, spirometry, and histamine challenge test. The evaluation of the work-relatedness of asthma in the exposed workers was based on serial peak expiratory flow rate (PEFR) measurements and bronchoprovocation tests. We found a higher prevalence of respiratory symptoms in the exposed workers, whereas spirometric parameters were significantly lower. The prevalence of sensitisation to allergens and of bronchial hyperresponsivenss (BHR) did not differ significantly between the groups. The prevalence of asthma was also similar in both groups (8.0 % vs. 6.4 %; P=0.540). Work-relatedness of symptoms was reported by all asthmatic tea workers and by no control with asthma. Significant work-related changes in PEFR diurnal variations and in non-specific BHR, suggesting allergic OA, were found in one tea worker with asthma (1.6 %). No specific workplace agent causing OA in the affected subject was identified. None of the tea workers with asthma met the criteria for medical case definition of the reactive airway dysfunction syndrome (RADS). Our data confirm workplace exposure to herbal and fruit tea dust as a risk factor for OA.     

Airway response to formaldehyde inhalation in asthmatic subjects with suspected respiratory formaldehyde sensitization

The aim of the study was to characterize the mechanism of formaldehyde (FM)-induced nasal and bronchial response in asthmatic subjects with suspected FM allergy. Ten subjects purported to have FM rhinitis and asthma and 10 healthy subjects submitted to an inhalation provocation in an exposure chamber with FM at a dose of 0.5 mg/m³ over 2 hr. Spirometry at rest and following bronchial provocation with histamine (PC₂₀) were recorded before and after FM inhalation. In addition, FM-specific serum IgE antibodies were measured and cellular, biochemical, and mediator changes were assessed in nasal lavage before, and immediately after, provocation and at 4 hr and 24 hr later. Provocation with FM caused only transient symptoms of rhinitis in both groups. None of the subjects supposed to have occupational asthma developed clinical symptoms of bronchial irritation. No specific IgE antibodies to FM were detected in persons with occupational exposure to FM. No differences in the nasal response to FM were found between subjects reporting to have occupational allergic respiratory diseases and healthy subjects (P > 0.05). In summary, inhaled formaldehyde at a level as low as 0.5 mg/m³ did not induce a specific allergic response either in the upper or in the lower part of the respiratory tract. Moreover, there is no difference in nasal response to FM in asthmatic subjects occupationally exposed to FM and healthy subjects. Am. J. Ind. Med. 33:274–281, 1998. © 1998 Wiley-Liss, Inc.     

Respiratory symptoms,ventilatory impairment,and bronchial reactivity in oil mist-exposed automobile workers

Studies concerning the respiratory effects of oil mists are sparse and contradictory. The aim of this study was to determine the respective effects of occupational exposure to straight cutting oils and soluble mineral oils on the prevalence of respiratory symptoms, ventilatory impairment, and bronchial reactivity. The population study consisted of 308 male workers of a large French car-making plant, including 40 subjects chronically exposed to straight cutting oils (group S), 51 subjects chronically exposed to soluble mineral oils (group E), 139 subjects with chronic dual exposure to straight cutting oils and soluble mineral oils (group D), and 78 unexposed assembly workers used as a control group (group C). Worker evaluation included a standardized questionnaire, measurement of pulmonary function, and a methacholine challenge. Oil mist concentration at the work place was determined by gravimetric analysis. The arithmetic mean concentration was 2.6 ± 1.8 mg/m³. The geometric mean concentration was 2.2 pm 1.9 mg/m³. The prevalence of respiratory symptoms did not differ significantly among the four groups. However, the subjects exposed to straight cutting oils (group S + group D) had a significantly higher prevalence of chronic cough and/or phlegm than the others (group E + group O): 25.7% vs. 16.3% (p = 0.048). Furthermore, the prevalence of cough and/or phlegm increased significantly (p = 0.03) with increasing duration of exposure to straight cutting oils after adjustment on smoking categories. Lung function tests did not differ significantly among the four groups but we observed a significant decrease of forced expiratory volume in 1 see (FEV₁), forced expiratory flow during the middle half of forced vital capacity (FEF_25-75), and maximal flow rate at 50% and 25% of exhaled forced vital capacity (V₅₀ and V₂₅) according to duration of exposure among smokers exposed to straight cutting oils, suggesting a synergistic effect of tobacco and insoluble oils. No effect of exposure to mineral oils on bronchial reactivity was demonstrated. It is concluded that despite low levels of pollution by oil mists, the present study has shown tenuous adverse chronic effects of straight cutting oils on respiratory symptoms and lung function. However, no adverse effect of soluble mineral oils was demonstrated. These results suggest that threshold limit values for mineral oils should be reassessed.     

Follow-up of airway reactivity in potroom workers in relation to exposure.

Two groups of workers were studied: a) 24 workers with respiratory complaints--7 of whom were light and 4 borderline hyper-reactors--who continued to work on the electrolytic reduction of aluminium for up to two years; b) 30 workers with increased bronchial reactivity who ceased to work in potrooms for 3.7 years on average (range 2-11 years) because of respiratory complaints. Subjective respiratory complaints were recorded and a non specific bronchial reactivity test was performed one or two times during the follow-up period. A sustained level of airway reactivity was recorded in both groups of workers regardless of exposure conditions. In workers with dyspnoea and airway obstruction, bronchial reactivity did not worsen in spite of continued exposure. On the other hand cessation of exposure was not followed by normalization of bronchial reactivity. The potential role of atopy, smoking habits and length of previous exposure was analyzed. It appears that increased bronchial reactivity, once induced, has a tendency to persist. An improvement in subjective complaints may be expected after cessation of exposure.     

Dietary Antioxidants and Ozone-Induced Bronchial Hyperresponsiveness in Adults with Asthma

Ozone exposure aggravates asthma, as has been demonstrated in both controlled exposures and epidemiologic studies. In the current double-blind crossover study, the authors evaluated the effects of dietary antioxidants (i.e., 400 IU vitamin E/500 mg vitamin C) on ozone-induced bronchial hyperresponsiveness in adult subjects with asthma. Seventeen subjects were exposed to 0.12 ppm of ozone or to air for 45 min during intermittent moderate exercise. Bronchial hyperresponsiveness was assessed with 10-min sulfur dioxide (i.e., 0.10 ppm and 0.25 ppm) inhalation challenges. Subjects who were given dietary antioxidants responded less severely to sulfur dioxide challenge than subjects given a placebo (i.e., forced expiratory volume in the 1st sec: -1.2% vs. 4.4%, respectively; peak flow: +2.2% vs. -3.0%, respectively; and mid-forced expiratory flow: +2.0% vs. -4.3%, respectively). Effects were more pronounced when subjects were grouped by response to sulfur dioxide at the screening visit. The results suggest that dietary supplementation with vitamins E and C benefits asthmatic adults who are exposed to air pollutants.     

Dietary antioxidants and ozone-induced bronchial hyperresponsiveness in adults with asthma

Ozone exposure aggravates asthma, as has been demonstrated in both controlled exposures and epidemiologic studies. In the current double-blind crossover study, the authors evaluated the effects of dietary antioxidants (i.e., 400 IU vitamin E/500 mg vitamin C) on ozone-induced bronchial hyperresponsiveness in adult subjects with asthma. Seventeen subjects were exposed to 0.12 ppm of ozone or to air for 45 min during intermittent moderate exercise. Bronchial hyperresponsiveness was assessed with 10-min sulfur dioxide (i.e., 0.10 ppm and 0.25 ppm) inhalation challenges. Subjects who were given dietary antioxidants responded less severely to sulfur dioxide challenge than subjects given a placebo (i.e., forced expiratory volume in the 1st sec: -1.2% vs. 4.4%, respectively; peak flow: +2.2% vs. -3.0%, respectively; and mid-forced expiratory flow: +2.0% vs. -4.3%, respectively). Effects were more pronounced when subjects were grouped by response to sulfur dioxide at the screening visit. The results suggest that dietary supplementation with vitamins E and C benefits asthmatic adults who are exposed to air pollutants.     

Exposure to hydrogen sulphide and respiratory function.

A study was carried out to assess possible effects of low concentrations of hydrogen sulphide on respiratory function. The cohort comprised 26 male pulp mill workers (mean age 40.3, range 22-60 years) with a daily exposure to hydrogen sulphide in the workplace, and 10 volunteers, who had asthma (three men, mean age 40.7, range 33 to 50 years, and seven women, mean age 44.1, range 31 to 61 years). The respiratory function of the pulp mill workers was monitored by measuring forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and bronchial responsiveness after at least one day off work and at the end of a workday. Bronchial responsiveness was tested by challenge with histamine. The 10 asthmatic subjects were exposed in laboratory conditions to 2 ppm of hydrogen sulphide for 30 minutes in an exposure chamber. Airway resistance (Raw) and specific airway conductance (SGaw) were assessed by a body plethysmograph, and the ventilatory capacities were measured with a flow volume spirometer. No significant changes in respiratory function or bronchial responsiveness related to exposure to hydrogen sulphide in the pulp mill workers were found. In the asthmatic subjects, Raw was increased by 26.3% and SGaw was decreased by 8.4% on average after exposure to hydrogen sulphide. These changes were not statistically significant. In two subjects, however, changes were greater than 30% in both Raw and SGaw, indicating bronchial obstruction. It is concluded that exposure for a relatively short time to hydrogen sulphide concentrations appreciably higher than those existing in ambient air do not cause noticeable effects on respiratory function.     

Airway hyper-responsiveness and the prevalence of work-related symptoms in workers exposed to irritants

The association between exposure to airway irritants and the presence of work-related symptoms and whether this association was modified by airway hyper-responsiveness, smoking, and allergy by history was studied in 668 workers of synthetic fiber plants. A Dutch version of the British Medical Research Council (BMRC) questionnaire with additional questions on allergy and work-related symptoms was used to assess symptoms, and a standardized histamine challenge test of airway hyper-responsiveness (AHR) was employed. Work-related symptoms were defined as having more than usual eye and respiratory symptoms during work. On the basis of job titles and working department, the exposure status of all workers was characterized into seven groups: (1) reference group; (2) white collars; (3) SO₂, HC1, SO₄ ^2-; (4) polyester vapor; (5) oil mist and oil vapor; (6) polyamide and polyester vapor; and (7) multiple exposure. The association between exposure groups and work-related symptom prevalence was estimated by means of multiple logistic regression. The overall prevalence of the work-related symptoms were: cough 9%; phlegm 6%; dyspnea 7%; wheeze 2%; eye symptoms 16%; nasal symptoms 15%. Exposure to airway irritants was significantly associated with work-related symptoms, independent of AHR, smoking, allergy by history, and chronic respiratory symptoms. The association of exposure group with work-related symptoms was stronger for subjects with AHR than for subjects with no AHR. The association with dyspnea and/or wheeze was also stronger for smokers than for nonsmokers and ex-smokers. In contrast, the association between exposure and a higher prevalence of work-related symptoms was stronger in subjects with no history of allergy than in subjects with history of allergy. This is most likely due to the relatively high prevalence of background symptoms in (nonexposed) allergic subjects. It is concluded that exposure to irritants in the working environment might lead to respiratory symptoms, even if exposure levels are relatively low.     

Exercise-induced bronchoconstriction and exercise-induced respiratory symptoms in workers exposed to tea dust

Assuming that airborne particles and pollutants are important contributing factors in the development of exercise-induced bronchoconstriction (EIB), we performed a case-control study including 63 tea workers (36 men and 27 women, aged 36-55, duration of employment 3-30 years) and an equal number of office workers, matched by sex and age. Exercise-induced respiratory symptoms were recorded in a questionnaire. Skin prick tests, spirometry, as well as exercise and histamine challenge were carried out. Environmental measurements were performed on site during the work shifts. The prevalence of self-reported exercise-induced respiratory symptoms and EIB did not differ significantly between the exposed and control group (41.6% vs 36.8%, and 6.4% vs 4.8%, respectively). In both exposed and control workers, EIB was strongly linked to asthma (P < 0.01). In the exposed workers it was significantly associated with positive family history of asthma (P < 0.01) and positive family history of atopies (P < 0.05), whereas in the exposed smokers it was significantly related to smoking duration (P < 0.05). Bronchial reaction to exercise in the exposed smokers was significantly greater than in control smokers (P < 0.05). Self-reported exercise-induced respiratory symptoms were weakly associated with EIB, with a large proportion of false positive and a low proportion of false negative results in both groups.     

Exposure to hydrogen sulphide and respiratory function

A study was carried out to assess possible effects of low concentrations of hydrogen sulphide on respiratory function. The cohort comprised 26 male pulp mill workers (mean age 40.3, range 22-60 years) with a daily exposure to hydrogen sulphide in the workplace, and 10 volunteers, who had asthma (three men, mean age 40.7, range 33 to 50 years, and seven women, mean age 44.1, range 31 to 61 years). The respiratory function of the pulp mill workers was monitored by measuring forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and bronchial responsiveness after at least one day off work and at the end of a workday. Bronchial responsiveness was tested by challenge with histamine. The 10 asthmatic subjects were exposed in laboratory conditions to 2 ppm of hydrogen sulphide for 30 minutes in an exposure chamber. Airway resistance (Raw) and specific airway conductance (SGaw) were assessed by a body plethysmograph, and the ventilatory capacities were measured with a flow volume spirometer. No significant changes in respiratory function or bronchial responsiveness related to exposure to hydrogen sulphide in the pulp mill workers were found. In the asthmatic subjects, Raw was increased by 26.3% and SGaw was decreased by 8.4% on average after exposure to hydrogen sulphide. These changes were not statistically significant. In two subjects, however, changes were greater than 30% in both Raw and SGaw, indicating bronchial obstruction. It is concluded that exposure for a relatively short time to hydrogen sulphide concentrations appreciably higher than those existing in ambient air do not cause noticeable effects on respiratory function.     

Partial protection by respirators on airways responses following exposure in a swine house

BACKGROUND: Exposure to swine dust leads to an intense airway inflammation and increased bronchial responsiveness. The purpose of the present study was to evaluate the effect of a respiratory protection device during exposure in a swine house. METHODS: Twenty-two subjects, 11 with a respirator, were exposed. Symptoms, body temperature, nasal lavage, and a bronchial metacholine challenge were performed before and 7 hr after exposure. For exposure assessment a nasal sampler was evaluated. RESULTS: The subjects with a respirator showed an attenuated inflammatory nasal response. An increase in bronchial responsiveness was observed in both groups, significantly greater in the unprotected group. The use of respirators reduced endotoxin exposure by more than 90% (assessed by nasal samplers). CONCLUSION: The use of a respirator attenuated the inflammatory response compared with an unprotected group. The minor effect on bronchial responsiveness suggests that gases and/or ultrafine particles may also be important factors.     

Airway hyperresponsiveness, prevalence of chronic respiratory symptoms, and lung function in workers exposed to irritants.

The association between occupational exposure to airway irritants and the prevalence of chronic respiratory symptoms and level of lung function, and whether these associations were modified by airway hyperresponsiveness, smoking, and a history of allergy were studied in 668 workers from synthetic fibre plants. Respiratory symptoms were recorded with a self administered Dutch version of the British Medical Research Council questionnaire, with additional questions on allergy. Airway responsiveness was measured by a 30 second tidal breathing histamine challenge test. On the basis of job titles and working department, the current state of exposure of all workers was characterised as (1) no exposure, reference group; (2) white collar workers; (3) SO2 HCl, SO4(2); (4) polyester vapour; (5) oil mist and vapour; (6) polyamide and polyester vapour; (7) multiple exposure. Workers exposed to airway irritants were not simultaneously exposed to airborne dust. Airway hyperresponsiveness (AHR), defined as a 20% fall in forced expiratory volume in one second (FEV1) at < or = 32 mg/ml histamine, was present in 23% of the subjects. The association between exposure groups and prevalence of symptoms was estimated by means of multiple logistic regression; the association with level of lung function (forced vital capacity (FVC), FEV1, maximum mid-expiratory flow rate (MMEF)) was estimated by means of multiple linear regression. Both methods allow simultaneous adjustment for potential confounding factors. The exposure groups were associated with a higher prevalence of chronic respiratory symptoms. Lower prevalence of symptoms was found for workers exposed to SO2, HCl, and SO4(2-), most likely due to pre-employment selection procedures. Current smoking, AHR, and a history of allergy were significantly associated with a higher prevalence of chronic respiratory symptoms, independent of each other, and independent of irritant exposure. The association between exposure and prevalence of symptoms was greater in smokers than in ex-smokers and non-smokers. This difference was most clearly seen in the polyester vapour and polyamide and polyester vapour group. No modification of the association between exposure groups and prevalence of symptoms by airway hyperresponsiveness could be shown. The exposure groups were not significantly associated with a lower level of lung function. Adjustment for chronic respiratory symptoms did not change the results. There were no indications of a possible interaction between exposure and AHR, current smoking, or a history of allergy on lung function. Workers of the polyester vapour and the oil mist and vapour group with >10 years of exposure had a lower FEV1 (beta = -295 and -358 ml) and significantly lower MMEF (beta = -1080 and -1247 ml/s; p < 0.05) than the reference group. The number of workers of both group were, however, small (n = 10 and n = 13 respectively). More investigations between low level exposure to irritant and respiratory health.