Inflammation in induced sputum after aluminium oxide exposure: an experimental chamber study.

INTRODUCTION: Workers in aluminium production are exposed to a complex mixture of particles and gases potentially harmful to the airways, among them aluminium oxide (Al2O3). With the use of an exposure chamber, we aimed to examine the effects of short-term controlled exposure to Al2O3 on lung function and inflammatory markers in healthy volunteers. METHODS: 15 men (age 19-31) were exposed in random order to clean air or Al2O3 particles (3.8-4.0 mg/m(3)) for 2 h including 30 min exercise (stationary bike, 75 W). The permissible exposure level (PEL) for Al2O3 by Occupational Safety and Health Administration, USA, is 5 mg/m(3) time weighted average (TWA). Sham and particle exposures were separated by at least 2 weeks. Spirometry was carried out, and induced sputum and blood samples were collected 48 h before and 4 and 24 h after exposure. RESULTS: Levels of sputum neutrophils (mean (±SEM)) was increased 24 h post-Al2O3 vs pre-Al2O3 exposure (43% (4) vs 31% (4), p=0.01) and the protein level of interleukin (IL)-8 had a 4.8 (0.9)-fold change increase 24 h after exposure (p<0.01). Following Al2O3 exposure, gene signatures in sputum were significantly increased related to several pathways. CONCLUSIONS: The present study suggests that controlled exposure to Al2O3 particles at levels below PEL (TWA) induces airway inflammation in healthy humans marked by elevated neutrophils and elevated IL-8. In addition, increased expression of genes associated with several biological processes was observed in sputum. Interestingly, inhaled Al2O3-induced effects were localised to the airways and not systemic.

Inflammatory markers in bronchoalveolar lavage fluid from human volunteers 2 hours after hydrogen fluoride exposure.

Fluoride has been in focus as a possible causal agent for respiratory symptoms amongst aluminium potroom workers for several decades. Previously, using bronchoalveolar lavage (BAL), we demonstrated airway inflammation in healthy volunteers 24 hours after exposure to hydrogen fluoride (HF). The objective of the present study was to examine early lung responses to HF exposure. Bronchoscopy with BAL was performed 2 hours after the end of 1-hour exposure to HE Significant reductions in the total cell number and the number of neutrophils and lymphocytes were observed in bronchoalveolar portion (BAP), whereas there were no significant changes in the bronchial portion (BP). Significantly decreased concentrations of beta2-MG, IL-6 and total protein were found in both BAP and BP. Additionally, IL-8 was significantly reduced in BP, and ICAM-1 and albumin were present in lower concentrations in BAP. Lung function measurements were not affected by HF exposure. These reported effects are presumably transitory, as many were not present in the airways 24 hours after a similar HF exposure.

Increased CD3 positive cells in bronchoalveolar lavage fluid after hydrogen fluoride inhalation.

OBJECTIVES: This study examined whether experimental hydrogen fluoride exposure for 1 hour induces an inflammatory response in the lower respiratory tract that is detectable in bronchoalveolar lavage fluid. METHODS: Nineteen healthy, nonsmoking men were exposed for 1 hour to constant low (<0.6 mg/m3), intermediate (0.7-2.4 mg/m3), or high (2.5-5.2 mg/m3) concentrations of hydrogen fluoride. Bronchoalveolar lavage was performed at least 3 weeks before and 24 hours after the exposure. For 15 subjects differential countings were performed. RESULTS: There was a significant increase in the percentage of CD3 positive cells in the bronchial portion for those exposed to "intermediate" and "high" concentrations. For the "high" exposure group the increase in the bronchoalveolar portion was also significant. A significant correlation was found between the increase in the percentage of lymphocytes and CD3 positive cells in the bronchoalveolar portion (Spearman's coefficient r=0.68, P=0.008). Myeloperoxidase and interleukin-6 increased significantly in the bronchial portion for those exposed to "high" concentrations. There was a significant increase in myeloperoxidase (P=0.005) for all the exposures, while there was a decrease in E-selectin (P=0.007). CONCLUSIONS: Hydrogen fluoride may induce an inflammatory reaction in the airways at concentrations that can occur in the ambient air in the primary aluminum industry.

Exposure to bacterial aerosols and work-related symptoms in sewage workers.

Personal exposure to airborne bacteria and symptoms were studied in 24 sewage workers. An association between levels of total bacteria, rod-shaped bacteria, and symptoms, such as tiredness and headache, during and after work was found.

A test chamber for experimental hydrogen fluoride exposure in humans.

An inhalation chamber was built to perform experimental studies with hydrogen fluoride (HF), other gases, and particulate matter. The present study sought to describe a new gas delivery system and the distribution and concentration of HF gas in the chamber. The aluminum chamber has a volume of 19.2 m3 and a variable ventilation rate of about 1 to 10 air changes per hour. The negative pressure difference between the chamber and outside air can be regulated from 0 to 300 Pa. HF was fed at concentrations of up to 4000 mg/m3 directly into the ventilation duct feeding the chamber through openings with diameters as small as 50 microns, oriented opposite to the airflow. Gas flow was varied from about 0.1 dm3/min at a pressure of 4 atm. The dilution factor of HF concentration from cylinder to chamber was on the order of 10(3) to 10(4). The standard deviation (SD) of the HF concentrations at a fixed measurement point during a 1-hour test was typically 0.05 mg/m3 at a time-weighted average (TWA) concentration of 2.66 mg/m3. The SD of the TWA HF concentrations at six locations in the chamber was typically 0.05 mg/m3 and 0.29 mg/m3 at 0.61 and 3.46 mg/m3, respectively. Human exposure could be predicted from calculations based on ventilation data, gas flow, and observed ratio between calculated and measured concentrations. When the target exposure concentration was 1.5 mg/m3, the measured mean exposure concentration was typically 1.54 mg/m3 (range: 1.4-1.7 mg/m3, SD 0.09 mg/m3, n = 8). The chamber is well-suited for inhalation studies in humans. Chamber atmosphere was controlled and has proved to be stable and homogeneous, even in tests with HF, a highly reactive gas in the class of superacids.

Hazardous peak concentrations of hydrogen sulfide gas related to the sewage purification process.

The concentration of hydrogen sulfide in the atmosphere of a sewage purification plant in Norway was studied. Continuous measurements over several 3-week periods showed that the concentrations generally were lower than 2 ppm, but peak concentrations over 100 ppm were discovered. Rapid onset and decline characterized these peak concentrations, which occurred at regular intervals. Through evaluation of the time pattern of these peaks compared with plant operations, a specific process was identified as the likely causative factor of the spikes. Through simple remedial actions the hydrogen sulfide concentration associated with this activity was reduced from above 100 ppm to less than 2 ppm. Olfactory fatigue to hydrogen sulfide and strong offensive odors from other compounds in the sewage makes smell ineffective for signaling high concentrations. Peak concentrations may therefore pass unnoticed unless detected with continuous measuring equipment. The risk for exposure may be reduced by enclosing processes and through the use of spot extraction ventilation in areas with compacted anaerobic waste material.

Exposure to hydrogen fluoride: an experimental study in humans of concentrations of fluoride in plasma, symptoms, and lung function.

OBJECTIVES: To study the absorption of inhaled hydrogen fluoride (HF) by measuring plasma fluorides and HF concentrations in the breathing zone during exposure to HF. A possible dose-effect relation was investigated by following airway symptoms and lung function-that is, forced expiratory volume in one second (FEV1) and forced vital capacity (FVC)-during and after exposure to HF. METHODS: 20 healthy, male volunteers were exposed for one hour to constant HF concentrations that ranged from 0.2 to 5.2 mg/m3; these concentrations are known to occur among potroom workers in the primary aluminium industry. Plasma fluorides were analysed before, during, and after exposure. Symptoms from the eyes and the upper and lower airways were registered and graded from 1 to 5 with a standardised questionnaire. RESULTS: The total symptom score was significantly increased at the end of exposure for all the subjects as a group (P < 0.01) and for the group exposed to HF below the present Norwegian standard for total fluorides 0.6 mg/m3 (P = 0.05). No change was detected in FEV15 although a significant decrease was found in FVC in the group exposed to fluorides below the hygienic standard (n = 9) and for the entire group (n = 23). Almost all the symptoms had disappeared four hours after the end of exposure. Symptom scores from the upper airways were significantly correlated with the HF concentration (r = 0.62, P = 0.002), the change in plasma fluoride concentration (delta C) (r = 0.51, P = 0.01), and the maximum plasma fluoride concentration (Cmax) (r = 0.42, P = 0.05). A significant correlation was also found between the total symptom score for airways and the HF concentration. CONCLUSIONS: The present study showed a strong relation between inhaled HF and concentrations of fluoride in plasma. Upper airway and eye symptoms occurred after one hour of exposure to HF even when below the Norwegian hygienic standard for fluorides.