Wood smoke in a controlled exposure experiment with human volunteers.

Exposure to wood smoke in the general population is increasing and concurrently, also our awareness. This article describes a wood-smoke generating system for studying human exposure to wood smoke and symptoms related to this exposure. Twenty nonsmoking atopic human participants with normal lung function and normal bronchial reactivity were randomly exposed for 3 h at three different exposure conditions; clean filtered air (control exposure) and wood smoke with a characteristic particulate matter (PM) concentration of 200 µg/m³ (low) and 400 µg/m³ (high) under controlled environmental conditions. The range for PM2.5 load observed for single experiments was 165-303 µg/m³ for the low exposure and 205-662 µg/m³ for the high exposure, whereas particle loads during clean air exposure most often were below the detection limit (< 20 µg/m³). Health effects were evaluated in relation to rated changes in symptoms and environmental perception using a computerized questionnaire and a potentiometer. Subjective symptoms were generally weak, but when combining the effect of each of the symptoms into categorical symptom indices, significant effects were found for "environmental perception" (p = 0.0007), "irritative body perceptions" (p = 0.0127), "psychological/neurological effects" (p = 0.0075) and "weak inflammatory responses" (p = 0.0003). Furthermore, significant effects (p = 0.0192) on self-reported general mucosa irritation were found. In conclusion, exposure to wood smoke affected symptom rating and caused irritated mucosas in humans. The knowledge gained in this study on subjective-rated symptoms may be important for understanding human response to wood-smoke exposure.

Nasal hyperresponders and atopic subjects report different symptom intensity to air quality: a climate chamber study.

UNLABELLED: Short-term exposure to dust and dust added with beta-(1,3)-d-glucan or aldehydes may cause sensory reactions. In random order, we exposed 36 volunteers in a climate chamber to clean air, office dust, dust with glucan, and dust with aldehydes. Three groups of subjects were exposed, eleven were non-atopic with nasal histamine hyperreactivity, 13 were non-atopic, and 12 were atopic. Subjective ratings of symptoms and general health were registered four times during four 6-h exposure sessions. Six symptom intensity indices were constructed. The nasal hyperreactive group had a high and time-dependent increase of mucous membrane irritations, whereas the atopic group had a low and stable rate of irritations with exposure time, close to the reference group (P = 0.02 for differences between the groups with respect to time under exposure for Weak Inflammatory Responses and P = 0.05 for Irritative Body Perception, significance mainly because of the nasal hyperreactive group). Exposure to dust, with or without glucan or aldehydes, showed increased discomfort measured by the index for Constant Indoor Climate, and dust with glucan had a similar effect for the index for Lower Respiratory Effects. For Psychological and Neurological Effects these were dependent on group affiliation, thus preventing a uniform statement of exposure effects for all three investigated groups. PRACTICAL IMPLICATIONS: Opportunities for identifying persons with high or low sensitivity to low-level exposures are important in preventive medicine and will reduce intra-group variability and thus increase the power of experimental and epidemiological studies searching for correlations between exposures and health effects. The contrast between nasal hyperreactive on one side and atopic and reference subjects on the other side is particularly important. The atopic group indicated a non-homogenous reaction depending on their hyperreactive status, a finding that could be important but needs further confirmation.

Effects on human eyes caused by experimental exposures to office dust with and without addition of aldehydes or glucan.

UNLABELLED: Thirty-six volunteers (in three susceptibility groups: 11 subjects were non-allergic with nasal histamine hypersensitivity, 13 were non-allergic with normal sensitivity, and 12 were pollen allergic with or without nasal hypersensitivity) were exposed for three and a half hours in a climate chamber. Each subject was exposed to clean air (dust 45 +/- 38 microg/m(3) total suspended particle, TSP), house dust at 357 +/- 180 microg/m(3) TSP, house dust 382 +/- 175 microg/m(3) TSP with added glucan (50 ng/m(3)) and house dust 394 +/- 168 microg/m(3) TSP with added aldehydes corresponding to a gaseous phase of 300 microg/m(3) in the air. The study was explorative by nature. No significant effects of exposures as such were seen on break-up time, conjunctival epithelial damage score and Trolox Equivalent Antioxidant Capacity (TEAC) in tear film and subjective ratings. However, in TEAC a significant different time course was seen during exposures to aldehyde-containing dust indicating a subacute and late response to the exposures. Perceived eye irritation increased significantly during exposures to normal dust. The perception ratings were highly correlated, whereas no correlation was found between the subjective responses and the objective measurements. PRACTICAL IMPLICATIONS: The findings indicate that measurement effects on the eyes are rather insensitive measures of short time effects of office dust exposures.

Interaction between ozone and airborne particulate matter in office air.

UNLABELLED: This study investigated the hypotheses that humans are affected by air pollution caused by ozone and house dust, that the effect of simultaneous exposure to ozone and dust in the air is larger than the effect of these two pollutants individually, and that the effects can be measured as release of cytokines and changes of the respiratory function. Experimental exposures of eight atopic but otherwise healthy subjects were performed in a climate chamber under controlled conditions. The three controlled exposures were about 75 microg/m3 total suspended particulate matter, 0.3 p.p.m. ozone, and the combination of these. The exposure duration was 3 h. The outcome measures were interleukins and cells in nasal lavages (NAL), respiratory function, bronchial metacholine responsiveness, rhinometry symptoms and general well-being in a questionnaire and time course of general irritation on a visual analogue scale. Indications of interactions between exposure types were demonstrated for peak expiratory flow (PEF) (P<0.05) and for discomfort symptoms (P<0.03). Non-significant interactions were found for the concentration of interleukin-8 in NAL. The combined exposure was found to cause significantly more effects than either ozone exposures or dust exposures. This is interpreted as indications of a potentiation caused by the combined exposures to dust and ozone. The findings in this study are based on a limited number of subjects and thus should not be over-interpreted. However, they support the hypothesis that ozone at relatively high concentrations interacts with dust exposures to cause decrements in PEF and increase in discomfort measures. PRACTICAL IMPLICATIONS: If confirmed at lower ozone and dust concentrations this finding could help to explain many problems with indoor air quality reported in offices throughout the world.

Respiratory effects of experimental exposure to office dust.

UNLABELLED: The aim of this experiment was to test if healthy persons respond to exposures to normal office dust with objective or subjective effects in a dose-related way. If they did, the importance of their personal characteristics should be investigated. This paper presents the results related to respiratory effects caused by exposures to office dust. The experiment compared the responses of 24 healthy non-sensitive adult subjects with no known hyperreactivity to exposure to normal office dust in the air at 136 and 390 microg/m3 with their responses in clean air. The exposure duration was 5.25 h in a climate chamber under controlled conditions. The dust had no major identifiable specific reactive compounds. There were no direct effects of dust exposures on nasal lavages or rhinometry. The overall indications of the experiment are that healthy subjects without any hypersensitive reactions seem to respond to exposure to house dust without specific reactive components. The only effect indicated was on eosinophil cationic protein in nasal lavages and peak flow. A delayed effect on peak expiratory flow was observed the day after the exposure. Other effects were seen but in opposite direction of expectations. Several deviations from the original design of the experiment prevent any definitive conclusions from being made from these findings before they have been confirmed in future experiments to come. PRACTICAL IMPLICATIONS: Reflecting the exploratory status of the study its major implication is to point at possible future hypotheses. The study implies that office dust may have an effect on occupants' lung function even at concentrations found in normal indoor environments. The influences of a multitude of response modifying variables were tested but no consistent pattern was found. The study does therefore not identify a specific risk group but suggests that among normal non-sensitized subjects most of the traditional risk factors can be rejected as single responsible risk factor.

Eye trigeminal sensitivity, tear film stability and conjunctival epithelium damage in 182 non-allergic, non-smoking Danes.

UNLABELLED: The population distributions of CO(2)-induced irritation sensitivity in the eyes (COI), tear film stability (break-up time, BUT), and epithelium damage (ED) and the relation of these to basic potential confounders were assessed in an age- and gender-stratified random sample of citizens in Aarhus County, Denmark. One hundred eighty-two non-allergic, non-smoking persons participated. A general health questionnaire and an indoor air questionnaire was filled out before the measurements. The BUT was non-normally distributed, as was COI at 16% CO(2) and single ED-scores. However, COI average for all levels was normally distributed and the total score for ED was only marginally deviating. BUT decreased, the threshold to CO(2) increased, and irritation intensity at CO(2) eye exposure decreased with increasing age. ED was increased among women. There were no internal relations between the three measures, but reduced BUT was seen among subjects rating high levels of exposure to dust, electrostatic fields, and dry air. ED decreased by perceived unpleasant odors and increased with experiences of high temperatures. CO(2) sensitivity increased by perceived draught, dry air, and noise exposure prior to measurements. Selection bias cannot be excluded and the results may therefore not be truly representative of the general population. However, the results may be used as reference data for future use of measurements of break-up time, epithelium defects, and CO(2) sensitivity of the eyes in the indoor air. PRACTICAL IMPLICATIONS: The most direct implication is that results can be used as reference level for measurements in problem buildings and for individual measurements. The reference can also be used in research and the other results as basis for future hypotheses and for support of existing hypotheses.

Ozone exposure decreases the effect of a deep inhalation on forced expiratory flow in normal subjects.

Sixteen healthy nonsmoking subjects (7 women), 21-49 yr old, were exposed in a climate chamber to either clean air or 300 parts/billion ozone on 4 days for 5 h each day. Before each exposure, the subjects had been pretreated with either oxidants (fish oil) or antioxidants (multivitamins). The study design was double-blind crossover with randomized allocation to the exposure regime. Full and partial flow-volume curves were recorded in the morning and before and during a histamine provocation at the end of the day. Nasal cavity volume and inflammatory markers in nasal lavage fluid were also measured. Compared with air, ozone exposure decreased peak expiratory flow, forced expiratory volume in 1 s, and forced vital capacity (FVC), with no significant effect from the pretreatment regimens. Ozone decreased the ratio of maximal to partial flow at 40% FVC by 0.08 +/- 0.03 (mean +/- SE, analysis of variance: P = 0.018) and at 30% FVC by 0.10 +/- 0.05 (P = 0.070). Ozone exposure did not significantly increase bronchial responsiveness, but, after treatment with fish oil, partial flows decreased more than after vitamins during the histamine test, without changing the maximal-to-partial flow ratio. The decreased effect of a deep inhalation after ozone exposure can be explained by changes in airway hysteresis relative to parenchymal hysteresis, due either to ozone-induced airway inflammation or to less deep inspiration after ozone, not significantly influenced by multivitamins or fish oil.

Effects in the eyes caused by exposure to office dust.

This Danish Office Dust Experiment compares the responses of 24 normal non-sensitive adult subjects to exposure to normal office dust in the air at 136 and 390 micrograms/m3 (median) and to their responses in clean air. The exposure duration was 5 1/4 h in a climate chamber under controlled conditions. The dust had no major identifiable specific reactive compounds. The overall conclusion is that healthy subjects without any hypersensitive reactions seem to respond to exposure to the house dust. The effects observed were all found in interaction with response modifying factors. The effects were a decrease in inflammatory cells in tear fluids, increased epithelium defects, and a decrease in break-up time. No effect was seen on eye reddening, or eye sensitivity to CO2. As no specific hypotheses could be specified before the study for the observed interactions, no definitive conclusions can be made. Furthermore, it seemed that there was no consistency in the interacting factors after the exposure and the next morning. A tentative analysis of the effects of the importance of personal characteristics showed that only a minority within the subject group may respond to the exposure. However, no common set of sensitivity measures could be defined for these responders.

Effect of renovating an office building on occupants' comfort and health.

An intervention study was performed in a mechanically ventilated office building in which there were severe indoor climate complaints among the occupants. In one part of the building a new heating and ventilation strategy was implemented by renovating the HVAC system, and a carpet was replaced with a low-emitting vinyl floor material; the other part of the building was kept unchanged, serving as a control. A comprehensive indoor climate investigation was performed before and after the intervention. Over a 2-week period, the occupants completed a daily questionnaire regarding their comfort and health. Physiological examinations of eyes, nose and lungs were performed on each occupant. Physical, chemical and sensory measurements were performed before and after the intervention. The renewal of the flooring material was performed after a sensory test of alternative solutions in the laboratory. Before the floor material was installed in the office building, a full-scale exposure experiment was performed in the laboratory. The new ventilation strategy and renovation of the HVAC system were selected on the basis of laboratory experiments on a full-scale mock-up of a cellular office. The severity of occupants' environmental perceptions and symptoms was significantly reduced by the intervention.

Effects on eyes and nose in humans after experimental exposure to airborne office dust.

To test sensory irritation symptoms and physiological effects on humans caused by airborne office dust, ten subjects were exposed to both clean air and airborne non-industrial office dust for 3 h in a climate chamber. The average dust concentration in exposure sessions was 394 micrograms/m3 total suspended dust (TSD). Tear film break-up time, foam formation in the eye canthus, conjunctival epithelial damage, nasal volume, and nasal minimal cross-sectional area were assessed. Tear film break-up time decreased significantly after dust exposure and nasal volume showed a tendency to decrease. In a questionnaire investigation, significant effects were found from the questions: "facial skin humidity", "throat irritation", "feeling needs of coughing", "dry nose", "concentration difficulty", and "headache". Additionally, the intensity of the questions "facial skin humidity", "dry nose", "body skin temperature", "sluggishness", and "sleepiness" worsened over time. A correlation analysis showed that perceived "air quality" was significantly correlated with "dry eyes", "eye irritation", "facial skin irritation", "nose irritation", and "feeling stressed by chamber occupancy" for subacute responses, and with "odor intensity" for acute responses. This supports that the perceived air quality may be a function of odor and irritation symptoms. A number of localized symptoms of irritation (e.g. dry nose, throat irritation, coughing) and of general symptoms (e.g. sluggishness, sleepiness, headache, ability to concentration) were mutually correlated acutely and subacutely. These results indicate that non-industrial office dust may cause physiological changes and sensory symptoms in eyes and nose and that these effects have different time courses.

The eye irritation and odor potencies of four terpenes which are major constituents of the emissions of VOCs from Nordic soft woods.

Eye goggles were used to estimate human thresholds for sensory eye irritation from four monoterpenes: (+)3-carene, (-)limonene and (+)alpha-pinene and (rac)alpha-terpineol all known as air pollutants emitted from wood. Only a ranking of the irritation thresholds relative to that of n-butanol is given. The measurements showed that the thresholds for eye irritation of the terpenes ranged from subthreshold to below 1,250 mg/m3. It appears that the irritation of 3-carene and limonene in contrast to the expectations was of the same size as or less than that of n-butanol. Too few subjects reported eye-irritation for alpha-pinene and alpha-terpineol to allow estimates of thresholds of these compounds which therefore have much less irritative potency than n-butanol, 3-carene, and limonene. The measurements of one terpene alcohol do not support the hypothesis that monoterpene alcohols, would have lower eye irritation threshold than monoterpene hydrocarbons. The sequence from strongest odorant to weakest was alpha-terpineol, 3-carene, n-butanol, limonene and alpha-pinene. In conclusion, the tested terpenes can probably be ruled out as cause of acute eye irritation indoors. The measured odor thresholds did not deviate from the few values reported in the literature.

Cytokine release from the nasal mucosa and whole blood after experimental exposures to organic dusts.

The aim of this study was to assess the cytokine response after nasal exposure to organic dusts. In a double blinded, crossover study five garbage workers with occupational airway symptoms and five healthy garbage workers were intranasally exposed to endotoxin (lipopolysaccharide LPS), beta-1,3-D-glucan (GLU), Aspergillus sp., compost or the saline dilute for 15 min. Nasal cavity volume and nasal lavage (NAL) were performed at baseline and 3, 6, 11 h postexposure. NAL was analysed with differential cell counts, cysteinyl-leukotrienes, tumour necrosis factor alpha, interleukin (IL)-1beta, IL-6 and IL-8. A whole blood assay on cytokine-release was performed with LPS and GLU. NAL cytokines neutrophils, lymphocytes and albumin increased significantly at 6 h after LPS exposure. GLU induced an increase in albumin and a slight increase in IL-1beta 6-11 h post exposure. In the WBA a significant increase in all cytokines after exposure to LPS as well as GLU was found. Significantly more cells were seen in NAL of the control group 6 h post LPS exposure. In conclusion lipopolysaccharide is the most potent inducer of inflammation in the nasal mucosa whereas compost and beta-1,3-D-glucan only induce minor changes. This reaction to lipopolysaccharide is attenuated in workers with occupational airway symptoms. In whole blood assay, however, beta-1,3-D-glucan also induces cytokine release, indicating a different protective effect of the nasal mucosa towards lipopolysaccharide and beta-1,3-D-glucan.

Reactions of healthy persons and persons suffering from allergic rhinitis when exposed to office dust.

OBJECTIVES: Reactions to airborne office dust among healthy subjects and subjects suffering from allergic rhinitis were investigated. METHODS: Twelve healthy and 11 subjects suffering from allergic rhinitis were exposed to clean air [17 (SD 2) microg/m3] and office dust [439 (SD 68) microg/m3] for 245 minutes. The effect measurements included subjective sensations (questionnaire and potentiometer ratings), mood scale, peak flow, bronchial provocation with histamine using forced expiratory volume in 1 second as the effect measure, nasal mucosal swelling, tear film stability, epithelial damage, foam formation in the eye canthus, threshold for eye irritation with carbon dioxide, eye redness, cellular content of conjunctival fluid, and an addition test for distraction. As many investigations were made and as many statistical analyses (including subgroup analyses) were carried out, the risk of mass significance appeared. This problem was dealt with using the Bonferroni correction for multiple significance tests. RESULTS: The mean ratings of the potentiometer were higher (the subjects showed more irritation) during the dust exposure. The objective investigations showed only indications of effects of dust exposure, and some of the indications were in biologically unexplainable directions. No difference in the reactions to dust was observed between the healthy subjects and the subjects suffering from allergic rhinitis. CONCLUSIONS: Dust does not seem to have objective or subjective effects on humans, as only indications of dust effects were found. Subjects suffering from allergic rhinitis do not appear to be a risk group in relation to dust exposure.

Time course of sensory eye irritation in humans exposed to N-butanol and 1-octene.

In this study, we investigated the time course effect of sensory eye irritation in 16 subjects exposed (i.e., eye only) to n-butanol and 1-octene. Half the subjects were exposed to n-butanol, and the remaining subjects were exposed to 1-octene. Each subject was studied on 5 different days; during each day each subject was exposed in three runs (i.e., run 1, run 2, and run 3) to a constant concentration of either n-butanol or 1-octene. We performed run 1 and run 3, both of which lasted 15 min each, to evaluate persistence in "sensitization." We performed run 2, which lasted 60 min, to study the time course of sensory irritation. Ratings of ocular irritation intensity were obtained continuously during all three runs. The exposure concentrations for n-butanol were 0 mg/m3, 300 mg/m3, 900 mg/m3, and 3 000 mg/m3, and the exposure concentrations for 1-octene were 0 mg/m3, 6 000 mg/m3, 10 400 mg/m3, and 18 000 mg/m3. During run 2, we observed a slight increase in perceived eye irritation intensity for the lower concentrations of 1-octene and for all exposure concentrations of n-butanol. However, the threshold for irritation was clearly exceeded for only the 1-octene 10 400-mg/m3 and 18 000-mg/m3 exposures. During these two exposures, the response increased 10-fold following 20-40 min of exposure during run 2, after which the response remained constant. We investigated the existence of persistence in "sensitization" by comparing intensity of responses between run 1 and run 3. Persistence in "sensitization" was apparent for only the 1-octene exposure.

Sensory eye irritation in humans exposed to mixtures of volatile organic compounds.

Eight subjects participated in a controlled eyes-only exposure study of human sensory irritation in ocular mucosal tissue. The authors investigated dose-response properties and the additive effects of three mixtures of volatile organic compounds. The dose-response relationships for these mixtures showed increases in response intensity as concentration increased. Replication of exposure did not result in significantly different dose- response relationships. Moreover, the result implied that components of the three mixtures interacted additively to produce ocular irritation, a result referred to as simple agonism. Finally, the authors addressed the comparability of two methods to measure sensory irritation intensity (visual analogue scale and a comparative scale). The results indicated that the two rating methods produced highly comparable results.

Cytological changes and conjunctival hyperemia in relation to sensory eye irritation.

In general, irritation is a physiological response to a chemical or physical stimulus involving objective changes (e.g., local redness and edema) and subjective sensations (e.g., pruritus and pain). The perception of an irritating stimulus in the eyes and the upper airways is called sensory irritation. Sensory irritation is a prevalent symptom in relation to complaints about indoor air quality. The intensity of perceived sensory irritation in humans has mainly been evaluated using psychophysical methods. However, perceived sensory irritation is dependent on the subject expressing the symptoms; that is, it is a subjective measure. This is a problem in assessment of irritation effects from air pollution or other factors, since the expression of the irritation symptoms may be biased by, for example, interaction with other people and odors. The subjectivity of the measures is an important complication in several studies dealing with problems regarding indoor air quality. The bias problems make it important to complement the psychophysical measurements of sensory irritation with objective assessments of irritation. In addition, only little is known about the association between sensory irritation and possible physiological/ pathological changes in the mucosal membranes in relation to studies of indoor air. Two studies (study 1 and study 2) were conducted to investigate changes in conjunctival hyperemia and conjunctival fluid cytology for subjects exposed to volatile organic compounds (VOCs) in their eyes only. Eight subjects participated in study 1. Each subject was exposed to three different mixtures of VOCs. A total of 16 subjects participated in study 2. Half of the subjects were exposed to 1-octene and the other half, to n-butanol. In both studies, photographs of bulbar conjunctiva were taken and conjunctival fluid was sampled before and after exposure. Moreover, the perceived irritation intensities were registered continuously during exposure. Overall, perceived irritation intensity and conjunctival hyperemia increased with increasing exposure concentrations, whereas cytological changes in the conjunctival fluid samples did not seen to be related to exposure concentration, perceived irritation, or changes in conjunctival hyperemia.

Integration in human eye irritation.

Today it is widely known and accepted that indoor air pollution can affect health. To ensure a healthy indoor climate through source control it is necessary to be able to predict how much of a source can be introduced into a building without unacceptable health and comfort effects. This paper describes a study of human eye irritation, which is part of a research program aimed at developing the use of sensory reference scaling in source characterization. In reference scaling the sensory eye irritation caused by exposure to polluted air is measured in terms of a concentration of a reference gas causing equivalent eye irritation intensity. The purpose of this study, therefore, was to estimate a possible difference in the magnitude of perceived sensory irritation between unilateral and bilateral exposure of human eyes. In each of four runs ten subjects were exposed to five progressive concentrations of CO2. In two of the runs the subjects were exposed unilaterally and in the other two runs the subjects were exposed bilaterally. In an analysis of variance no significant difference was found between unilateral and bilateral exposures. As expected, the intensity of the perceived irritation increased significantly with increasing exposure level. The sensitivity decreased slightly but significantly following previous exposures. These results enable us to develop a model for source characterization in which sensory eye irritation is measured by reference scaling. The use of reference scaling has the advantage that an otherwise subjective response (perceived irritation intensity) becomes less biased.

Clinical studies of effects of nitrogen oxides in healthy and asthmatic subjects.

Traffic and cooking and heating using unventilated gas appliances are the major sources for environmental exposures to nitrogen oxides. The nitrogen oxides of importance for health effects are nitrogen dioxide (NO2), and maybe the two derivatives nitric and nitrous acid (HNO3 and HNO2). Due to this, human exposure studies on NO2 have been performed intensively during the last decades. Nitric oxide (NO) is quantitatively the major pollutant, but is not very toxic and may even be used in treatment of certain conditions of respiratory insufficience. Major lung function effects shown in humans are a decrease in the forced expiratory volume in the first second (FEV1), increased specific airway resistance (SRaw), and increased responsiveness in bronchial provocation tests. Studies have been performed primarily on healthy and asthmatic subjects, but only asthmatic subjects show these reactions at levels relevant to exposures found in indoor and outdoor environments. Other effects found in animal studies and epidemiological studies like decreased mucociliary function, increased susceptibility to infections have not been proven in humans and are therefore still on debate. Human studies have furthermore shown that antioxidants like vitamin C and E may prevent effects of NO2, which is explained by that the mechanism of NO2-action is the oxidation of airway phospholipids. A large inconsistency in the results of the studies makes it very difficult to conclude about dose-response relationships and about no observed effect levels (NOEL). Single study observations and results of meta-analyses have indicated a biphasic dose-response relationship. However, such a relationship is hard to explain and need to be investigated further. Several other explanations, e.g. the limited statistical power of the studies, may exist and will be discussed.

Frequency response of variable orifice type peak flow meters: requirements and testing.

Little is known about the response of variable orifice peak flow meters to high frequency flow input. The purpose of this study was to define and test dynamic requirements for such peak flow meters. In a population sample we measured peak expiratory flow (PEF), rise time (tr), from 10-90% PEF and the duration of the flow in excess of 97.5, 95 and 90% of PEF, by use of a carefully calibrated Fleisch pneumotachograph with known and adequate frequency response. Three peak flow meters (Mini Wright, Vitalograph and Ferraris) were tested with an explosive decompression calibrator adjusted to values for PEF and tr as close as possible to the 95th and 5th percentile values, respectively, both for males and females, and with peak durations between 5 and more than 100 ms. The 95th percentile values of PEF were 597 L.min-1 for females and 894 L.min-1 for males. The 5th percentile values of tr were, respectively 55 and 45 ms. The duration of flow in excess of 95% PEF was longer than 10 ms in 99% of the subjects. For all meters, the deviation of PEF corrected for alinearity were less than 5% at a peak duration of 10 ms. We conclude that PEF, rise time, and peak duration can be used for description of dynamic properties of variable orifice meters, and that the tested meters had a satisfactory frequency response for recording PEF in mostly normal subjects.

[Effects of low concentrations of NO2 on alveolar permeability and glutathione peroxidase in healthy subjects]. / Virkninger af mindre NO2-koncentrationer på alveolaer permeabilitet og glutationperoxidase blandt raske mennesker.

Potential toxic effects of prolonged NO2 exposure below the current threshold limit value (TLV) were examined in 14 healthy, non-smoking adults. The subjects were exposed to 2,3 ppm NO2 and to clean air for five hours with a one week interval between exposures. Physiological and biochemical measurements were obtained during exposure and the following 24 hours after. A 14% decrease in serum glutathione peroxidase activity (GSH-Px) was observed 24 hours after the start of the NO2 exposure while indications of a 22% decrease in alveolar permeability were found 11 hours after the start. There were no indications of mucous membrane irritation or of decreased lung function during or after NO2 exposures. The results support the assumption that a delayed response is a feature of the human reaction to NO2 even below the current TLV of three ppm, and they stress the importance of an extended period of observation in future NO2 exposure studies.