Respiratory Tract Irritation Research Articles

Psychophysical methods in the study of olfaction and respiratory tract irritation.

This article describes the fundamentals of olfaction and irritation perception and the dominant psychophysical methods for the assessment of olfaction and respiratory tract irritation. It also discusses factors that determine the olfactory and irritant response (ranging from the physicochemical properties of the stimulus to the physiological and cognitive characteristics of the individual). Because the vast majority of volatile chemicals stimulate the olfactory system at concentrations well below that at which they will elicit trigeminal activation, the evaluation of irritation from volatiles is often confounded by the perception of odor. Several methods have been used for studying the perception of irritation, without the influence of olfaction. The perception and reports of acute adverse effects of odor, annoyance, and irritation from volatile chemicals have multiple determinants. Understanding the perceptual impact of chemicals under environmentally realistic conditions requires attending to both the sensory and the psychological impact of those exposures. The review, which is largely based on presentations given by Dr. Richard Doty and Dr. William Cain, concludes by discussing the importance of the psychophysical approach, which considers physiochemical, subject, experimental, and cognitive/ psychological factors, for research in the chemical senses.

Psychophysical Methods in the Study of Olfaction and Respiratory Tract Irritation

Psychophysical Methods in the Study of Olfaction and Respiratory Tract Irritation

Approaches and considerations for setting occupational exposure limits for sensory irritants: report of recent symposia.

Over the past 50 years significant strides have been made in reducing occupational exposure to airborne chemicals. To a large extent, the impetus behind the reductions has been the identification of presumably safe levels of exposure, or occupational exposure limits (OELs). Most of the reduction in exposure has been to chemicals such as hepatotoxins, neurotoxins, nephrotoxins, and carcinogens that cause frank toxic effects. Recently, however, a number of industrial hygiene and occupational medicine initiatives have sought to identify acceptable levels of exposure to sensory irritants and reduce exposure to this class of chemicals. This article presents an overview of the field with emphasis on the work presented at two symposia sponsored by the Chemical Manufacturers Association: "How Do We Set an Occupational Exposure Limit (OEL) for Irritation?" (1998) at the American Industrial Hygiene Conference and Exposition and "Respiratory Tract Irritation and Olfaction Conference" (1997). The two symposia reviewed clinical and experimental methods used to assess odor and sensory irritation, to increase understanding of the research needed to establish OELs for sensory irritants, and to discuss how to use this information to identify appropriate values. The symposia illustrated that research in this area is evolving quickly and that there is already sufficient understanding to permit scientists to identify chemicals likely to be sensory irritants. Further, there appears to be an ample number of research methods for identification of airborne concentrations that should protect most workers. This article summarizes some of the key points raised at these symposia and suggests areas deserving of future study.

Assessment of pentachlorophenol-exposed timber workers using a test-of-poisoning model.

Sixty-two former New Zealand timber workers who were exposed to pentachlorophenol (PCP) at work were interviewed, examined, and assessed both by laboratory investigations and psychometrically for clinical syndromes that could be related to PCP exposure. Three such syndromes were identified: an acute complex of fever, headaches, upper and lower respiratory tract and eye irritation, skin disease, and foul smelling and discolored sweat; a chronic fatigue syndrome, beginning while still at work and frequently persisting; and a delayed encephalopathy. Neither of the sustained syndromes was considered characteristic of PCP poisoning, and many confounders were identified. An exposure index and a test-of-poisoning score had a statistically insignificant correlation.

“Smoke pH”: A Review

Abstract The analytical methods developed since the 1950s to determine the “smoke pH” of cigarette mainstream smoke (MSS) are reviewed. Most of the methods involve averaging the values obtained with all the puffs from a cigarette or averaging values from the total number of puffs from several cigarettes plus solution of the MSS in various quantities of water prior to pH determination. “Smoke pH” values thus obtained have little relevance to the situation involving a smoker who smokes a cigarette one puff at a time. In the human biological situation, the smoke components must traverse a layer of buffered fluid separating the smoke-filled respiratory tract cavity and the underlying tissue. Seldom is the effect of either the volume or the pH of the buffered fluid taken into account in determining the “smoke pH” of cigarette MSS taken one puff at a time. While numerous recent discussions have dealt with the effect of pH on the nature (degree of protonation) of nicotine in cigarette MSS and its rate of absorption by the smoker, seldom is the volume and/or pH of oral cavity saliva or of the fluid coating the lung surface considered in the assessment of either the nature or absorption of nicotine by the smoker. If the degree of protonation of nicotine be pH dependent, then the degree of protonation of nicotine as it traverses the film of fluid separating the respiratory tract cavity and the underlying tissue must be dependent on the pH of the buffered fluid and not on the “smoke pH” per se. Statements that adjustment of the “smoke pH” by ammoniation of one or more tobacco blend components increases both the level of MSS nicotine and its rate of absorption, thus resulting in greater consumer acceptance and continuation of smoking, fail to take into account the other changes that occur in the MSS composition to enhance its consumer acceptability. Inclusion of modest percentages of ammoniated tobacco in the blend increases the “smoke pH” of the MSS but does not necessarily increase MSS nicotine level. Not only are the MSS levels of several low molecular acids, aldehydes, and ketones known to be respiratory tract irritants substantially reduced but also the MSS levels of several highly flavorful pyrazines are substantially increased. These MSS composition changes yield an MSS classified as milder and more flavorful and whose consumer acceptability is considerably enhanced. Until the pH of MSS is determined on a per puff basis in a system simulating that in the oral cavity or the lung of the smoker, the nature of specific smoke components at the time of contact and their reactivity with respiratory tract tissue remain highly speculative. “Smoke pH” value for MSS, like the “tar” value for MSS, provides little, if any, useful information about the chemical composition of the source of the MSS or about its chemical and biological properties.

Human Safety and Pharmacokinetics of the CFC Alternative Propellants HFC 134a (1,1,1,2-Tetrafluoroethane) and HFC 227 (1,1,1,2,3,3,3-Heptafluoropropane) Following Whole-Body Exposure

HFC 134a (1,1,1,2-tetrafluoroethane) and HFC 227 (1,1,1,2,3,3,3-heptafluoropropane) are used to replace chlorofluorocarbons (CFCs) in refrigerant and aerosol applications, including medical use in metered-dose inhalers. Production and consumption of CFCs are being phased out under the Montreal Protocol on Substances that Deplete the Ozone Layer. The safety and pharmacokinetics of HFC 134a and HFC 227 were assessed in two separate double-blind studies. Each HFC (hydrofluorocarbon) was administered via whole-body exposure as a vapor to eight (four male and four female) healthy volunteers. Volunteers were exposed, once weekly for 1 h, first to air and then to ascending concentrations of HFC (1000, 2000, 4000, and 8000 parts per million (ppm)), interspersed with a second air exposure and two CFC 12 (dichlorodifluoromethane) exposures (1000 and 4000 ppm). Comparison of either HFC 134a or HFC 227 to CFC 12 or air gave no clinically significant results for any of the measured laboratory parameters. There were no notable adverse events, there was no evidence of effects on the central nervous system, and there were no symptoms of upper respiratory tract irritation. HFC 134a, HFC 227, and CFC 12 blood concentrations increased rapidly and in an exposure-concentration-dependent manner, although not strictly proportionally, and approached steady state. Maximum blood concentrations (Cmax) tended to be higher in males than females; in the HFC 227 study, these were statistically significantly (P < 0.05) higher in males for each HFC 227 and CFC 12 exposure level. In the HFC 134a study, the gender difference in Cmax was only statistically significant (P < 0.05) for CFC 12 at 4000 ppm and HFC 134a at 8000 ppm. Following the end of exposure, blood concentrations declined rapidly, predominantly biphasically and independent of exposure concentration. For the HFC 134a study, the t1/2α (α elimination half-life) was short for both CFC 12 and HFC 134a (<11 min). The t1/2β (β elimination half-life) across all exposure concentrations was a mean of 36 and 42 min for CFC 12 and HFC 134a, respectively. Mean residence time (MRT) was an overall mean of 42 and 44 min for CFC 12 and HFC 134a, respectively. In the HFC 227 study, t1/2α for both CFC 12 and HFC 227, at each exposure level, was short (<9 min) and tended to be lower in males than females. For CFC 12 mean t1/2β ranged from 23 to 43 min and for HFC 227 the mean range was 19–92 min. The values tended to be lower for females than males for HFC 227. For both CFC 12 and HFC 227, MRT was statistically significantly lower (P < 0.05) in males than females and independent of exposure concentration. For CFC 12, MRT was a mean of 37 and 45 min for males and females, respectively, and for HFC 227 MRT was a mean of 36 and 42 min, respectively. Exposure of healthy volunteers to exposure levels up to 8000 ppm HFC 134a, 8000 ppm HFC 227, and 4000 ppm CFC 12 did not result in any adverse effects on pulse, blood pressure, electrocardiogram, or lung function.

Effects of methacrolein on the respiratory tract in mice

The acute respiratory effects of airborne exposure to methacrolein were studied in a recent refinement of the standard test method with mice (ASTM, 1984. American Society for Testing and Materials, Philadelphia). Irritation of the upper respiratory tract caused a concentration-dependent decrease in the respiratory rate of 2–26 ppm methacrolein. In this range, only a minor airflow limitation occurred in the lower respiratory tract, suggesting that the main effect of methacrolein is sensory irritation. During exposure, the sensory irritation response maintained the same level, i.e. no desensitisation occurred. The concentration 10.4 ppm methacrolein reduced the respiratory rate by 50% (RD50). The extrapolated threshold for the respiratory depressing effect, RD0, was 1.3 ppm. The sensory irritation effect of methacrolein was compared with results from closely related compounds in order to elucidate the mechanism of the interaction between methacrolein and the sensory irritant receptor.

Respiratory toxicity of mattress emissions in mice.

Groups of male Swiss-Webster mice breathed emissions of several brands of crib mattresses for two 1-hr periods. The authors used a computerized version of ASTM-E-981 test method to monitor respiratory frequency, pattern, and airflow velocity and to diagnose abnormalities when statistically significant changes appeared. The emissions of four mattresses caused various combinations of upper-airways irritation (i.e., sensory irritation), lower-airways irritation (pulmonary irritation), and decreases in mid-expiratory airflow velocity. At the peak effect, a traditional mattress (wire springs with fiber padding) caused sensory irritation in 57% of breaths, pulmonary irritation in 23% of breaths, and airflow decrease in 11% of breaths. All mattresses caused pulmonary irritation, as shown by 17-23% of breaths at peak. The largest airflow decrease (i.e., affecting 26% of the breaths) occurred with a polyurethane foam pad covered with vinyl. Sham exposures produced less than 6% sensory irritation, pulmonary irritation, or airflow limitation. Organic cotton padding caused very different effects, evidenced by increases in both respiratory rate and tidal volume. The authors used gas chromatography/mass spectrometry to identify respiratory irritants (e.g., styrene, isopropylbenzene, limonene) in the emissions of one of the polyurethane foam mattresses. Some mattresses emitted mixtures of volatile chemicals that had the potential to cause respiratory-tract irritation and decrease airflow velocity in mice.

Environmental exposure to manganese and combined exposure to gaseous upper respiratory irritants: mechanism of action and adverse health effects.

This review relates to possible explanations of the often-observed findings that exposure to certain air pollutants or their mixture results in an increased rate of acute respiratory diseases. Epidemiological investigations have shown that exposure to manganese (MnO2) concentrations only 10 to 50 times higher than the normal urban concentrations of 0.01 to 0.03 microgram/m3 air might have an adverse health effect on respiratory organs. The assumption that one possible mechanism of action could be that manganese at such exposure levels disturbs certain protective functions in the lung--thus making the organism more susceptible to infections--is supported by toxicological studies. In vitro studies have demonstrated the cytotoxic action of manganese, including the inhibition of activities of alveolar macrophages. Animal experiments showed a decrease in resistance toward respiratory infections that were caused by simultaneous exposure to MnO2 and pathogenic bacteria. In cases of combined exposure to gaseous upper respiratory tract irritants and suspended particles, the involvement of adsorption of gaseous compounds on solid particles as carriers has been suggested. The assumption is that through such a mechanism, water-soluble gaseous irritants can be transported deep into air passages, which such irritants normally do not reach. As the adsorption is reversible, the gaseous compounds can later be released from the particles, inducing a local irritating effect in the small airways and alveoli.

Workplace Environmental Tobacco Smoke Exposure and Acute Airway Responses

Workplace exposure to environmental tobacco smoke (ETS) is common, affecting 17% of U.S. adults. Workers in certain occupations have an even higher prevalence of ETS exposure, especially food service, construction trades, and mechanics. In many workplaces, such as bars, restaurants, and airlines, concentrations of airborne nicotine and other ETS constituents reach particularly high levels. The California time-activity survey indicated that the workplace was the major site of total ETS exposure for nonsmoking men (46% of total person-minutes of exposure) and women (35% of person-minutes), followed by home exposure (15% and 20%, respectively). Workplace ETS exposure has been linked with acute upper respiratory tract and corneal mucous membrane irritation, resulting in eye, nose, and throat irritation symptoms. Workplace ETS exposure has also been associated with lower respiratory tract symptoms, impaired lung function, and exacerbation of adult asthma. Since workplace smoking prohibition effectively reduces ETS exposure, such policies should confer substantial short- and long-term public health benefits.

Sensory irritating potency of some microbial volatile organic compounds (MVOCs) and a mixture of five MVOCs.

The authors investigated the ability/potencies of 3 microbial volatile organic compounds and a mixture of 5 microbial volatile organic compounds to cause eye and upper respiratory tract irritation (i.e., sensory irritation), with an animal bioassay. The authors estimated potencies by determining the concentration capable of decreasing the respiratory frequency of mice by 50% (i.e., the RD50 value). The RD50 values for 1-octen-3-ol, 3-octanol, and 3-octanone were 182 mg/m3 (35 ppm), 1359 mg/m3 (256 ppm), and 17586 mg/m3 (3360 ppm), respectively. Recommended indoor air levels calculated from the individual RD50 values for 1-octen-3-ol, 3-octanol, and 3-octanone were 100, 1000, and 13000 microg/m3, respectively-values considerably higher than the reported measured indoor air levels for these compounds. The RD50 value for a mixture of 5 microbial volatile organic compounds was also determined and found to be 3.6 times lower than estimated from the fractional concentrations and the respective RD50s of the individual components. The data support the conclusion that a variety of microbial volatile organic compounds may have some synergistic effects for the sensory irritation response, which constrains the interpretation and application of recommended indoor air levels of individual microbial volatile organic compounds. The results also showed that if a particular component of a mixture was much more potent than the other components, it may dominate the sensory irritation effect. With respect to irritation symptoms reported in moldy houses, the results of this study indicate that the contribution of microbial volatile organic compounds to these symptoms seems less than previously supposed.

New inhalation agents in paediatric anaesthesia

A survey in August 1995 showed that, despite the introduction of topical analgesic creams, approximately 30% of anaesthetists responding used inhalation induction of anaesthesia more frequently than i.v. induction, especially in children less than 3–5 yr of age.9 In this age group, uptake of inhaled agents is particularly rapid. In children therefore, the induction characteristics of the ideal inhalation agent are particularly important although clearly the recovery profile, cardiovascular stability, minimal metabolism, stability in soda lime, lack of central nervous system excitation and antiemetic effect during recovery are as important as they are in adults (Table 1). Although cyclopropane provided rapid smooth induction, the risk of explosions led to its withdrawal from anaesthetic practice. In recent years, halothane has been accepted widely as the least pungent of the inhalation agents available, giving the smoothest induction with minimal risk of laryngospasm and hypoxaemia. Its disadvantages are well known and include myocardial irritability, especially in the presence of epinephrine, depression of myocardial and respiratory function, cerebral vasodilatation, biotransformation and rarely hepatotoxicity. Lack of familiarity with its use in adult practice by younger anaesthetists must now be added to this list of disadvantages. Two new inhalation agents have recently become available in this country: sevoflurane and desflurane. Both are fluorinated ethers, and as fluorine has 0.001% of the ozonedepleting activity of chlorine, both of these new drugs should be more environmentally friendly than halothane. Sevoflurane is relatively non-pungent, so that the vaporizer may be set to its maximum setting from the start of induction.77 Desflurane, however, is extremely pungent and causes severe irritation of the upper respiratory tract if used for induction of anaesthesia. Although desflurane is therefore not recommended for inhalation induction, there has been some recent interest in its use as a maintenance agent in infants, because of its shorter recovery time.65

Health effects of the 1991 Kuwait oil fires: a survey of US army troops.

The burning of oil wells in Kuwait in 1991 discharged a high volume of potentially toxic pollutants into the air. To determine whether there were health-related complaints associated with having lived and worked there, questionnaires were administered to 1599 soldiers after their return from a 3-month mission in Kuwait. Symptoms occurring before, during, and after the mission were queried. Compared with baseline, symptoms reported more frequently for the Kuwait period were eye and upper respiratory tract irritation, shortness of breath, cough, rashes, and fatigue. Symptoms were associated with reported proximity to oil fires, and their incidence generally decreased after the soldiers left Kuwait. Oil-fire smoke is one of several possible factors that may have contributed to the reporting of symptoms.

UPTAKE, TISSUE DISTRIBUTION, AND EXCRETION OF BREVETOXIN 3 ADMINISTERED TO RATS BY INTRATRACHEAL INSTILLATION

Brevetoxins are cyclic polyether neurotoxins produced by the marine dinoflagellate Ptychodiscus brevis. Blooms of P. brevis (red tides) are toxic to fish, marine mammals, and humans. Humans exposed to seaspray aerosols containing brevetoxins may experience respiratory tract irritation. Because a major route of human exposure to brevetoxins is via the respiratory tract, the objective of this study was to examine the toxicokinetics of brevetoxin 3 (PbTx-3) administered to the lung by intratracheal instillation. Twenty-one male F344/Crl BR rats, 12 wk of age, were administered 3H-PbTx-3 (1 muCi, 6.6 mug PbTx-3/kg) by intratracheal instillation. Groups of 3 rats were sacrificed at 0.5, 3, 6, 24, 48, and 96 h after exposure, and tissues were collected. Three additional rats were placed in glass metabolism cages for collection of urine and feces over a 7-d period. PbTx-3-associated activity was cleared rapidly from the lung and distributed throughout the body, chiefly to the carcass, intestines, and liver. Blood, brain, and fat contained the lowest percentages of the administered dose. Although a majority of the PbTx-3 was cleared rapidly from lung, liver, and kidneys, approximately 20% of the initial concentration present in each organ was retained for 7 d. Concentrations of PbTx-3 in brain and fat were low, but remained relatively constant over time. Approximately twice as much PbTx-3-associated activity was excreted in feces than in urine, with the majority of excretion occurring within 48 h after instillation. The results of this study indicate that over 80% of the PbTx-3 is rapidly absorbed from the lung to the blood and distributed to all tissues. The tissues containing the greatest amount of PbTx-3-associated activity reflect the compound's site of deposition, storage compartment, and major route of metabolism and excretion. These results illustrate that brevetoxin exposure by the respiratory route results in systemic distribution of brevetoxin and suggest that the initial respiratory irritation and bronchoconstriction may only be a part of the overall toxicological consequences associated with brevetoxin inhalation.

Vanadium.

Vanadium is a steel-grey, corrosion-resistant metal, which exists in oxidation states ranging from -1 to +5. Metallic vanadium does not occur in nature, and the most common valence states are +3, +4, and +5. The pentavalent form (VO3-) predominates in extracellular body fluids whereas the quadrivalent form (VO+2) is the most common intracellular form. Because of its hardness and its ability to form alloys, vanadium (i.e., ferrovanadium) is a common component of hard steel alloys used in machines and tools. Although most foods contain low concentrations of vanadium (< 1 ng/g), food is the major source of exposure to vanadium for the general population. High air concentrations of vanadium occur in the occupation setting during boiler-cleaning operations as a result of the presence of vanadium oxides in the dust. The lungs absorb soluble vanadium compounds (V2O5) well, but the absorption of vanadium salts from the gastrointestinal tract is poor. The excretion of vanadium by the kidneys is rapid with a biological half-life of 20-40 hours in the urine. Vanadium is probably an essential trace element, but a vanadium-deficiency disease has not been identified in humans. The estimated daily intake of the US population ranges from 10-60 micrograms V. Vanadyl sulfate is a common supplement used to enhance weight training in athletes at doses up to 60 mg/d. In vitro and animal studies indicate that vanadate and other vanadium compounds increase glucose transport activity and improve glucose metabolism. In general, the toxicity of vanadium compounds is low. Pentavalent compounds are the most toxic and the toxicity of vanadium compounds usually increases as the valence increases. Most of the toxic effects of vanadium compounds result from local irritation of the eyes and upper respiratory tract rather than systemic toxicity. The only clearly documented effect of exposure to vanadium dust is upper respiratory tract irritation characterized by rhinitis, wheezing, nasal hemorrhage, conjunctivitis, cough, sore throat, and chest pain. Case studies have described the onset of asthma after heavy exposure to vanadium compounds, but clinical studies to date have not detected an increased prevalence of asthma in workers exposed to vanadium.

TWO-WEEK INHALATION TOXICITY OF POLYMERIC DIPHENYLMETHANE-4,4'-DIISOCYANATE (PMDI) IN RATS: Analysis of Biochemical and Morphological Markers of Early Pulmonary Response

The pulmonary response of Wistar rats to respirable polymeric diphenylmethane-4,4'-diisocyanate (PMDI) aerosol was examined in a 2-wk repeated nose-only inhalation exposure study. Exposure concentrations were 1.1, 3.3, and 13.7 mg PMDI/m3 (6 h/day, 15 exposures). The level of 13.7 mg/m3 was actually a combination of an initial target concentration of 10 mg/m3 in wk 1, which was raised to 16 mg/m3 in wk 2, due to a lack of signs suggestive of pulmonary irritation. An acute sensory irritation study on rats served as basis for selection of these concentrations. Shortly after the 2-wk exposure period, rats were subjected to pulmonary function and arterial blood gas measurements. Lungs were examined by light and transmission electron microscopy, and labeling indices in terminal bronchioles were measured. Bronchoalveolar lavage (BAL) was performed to assess various indicators of pulmonary inflammation, including neutrophil and macrophage numbers, protein, lactate dehydrogenase (LDH), gamma-glutamyltranspeptidase (gamma-GT), alkaline phosphatase (APh), acid phosphatase (ACPh), and beta-N-acetylglucosaminidase (beta-NAG). Phosphatidylcholine in BAL fluid and BAL cells was determined as aggregated endpoint suggestive of changes in pulmonary surfactant. Rats exposed to 3.3 and 13.7 mg/m3 experienced concentration-dependent signs of respiratory tract irritation. Determination of arterial blood gases, lung mechanics, and carbon monoxide diffusing capacity did not demonstrate specific effects. Analysis of BAL fluid and BAL cells revealed changes indicative of marked inflammatory response and/or cytotoxicity in rats exposed to 13.7 mg/m3, and the changes were characterized by statistically significantly increased activities of LDH, beta-NAG, and protein. Phospholipid concentrations were increased in rats exposed to 1.1 mg/m3 and above (elevated levels of lipid material in alveolar macrophages demonstrated by polychrome stain) and 3.3 mg/m3 and above (increased intracellular ACPh activity and intracellular phospholipids). In these groups, gamma-GT was statistically significantly increased. These findings suggest that changes in phospholipid homeostasis appear to occur at lower levels than those eliciting inflammation and cytotoxicity. Light and transmission electron microscopy suggest that exposure to 3.3 and 13.7 mg/m3 resulted in focal inflammatory lesions and an accumulation of refractile, yellowish-brownish material in alveolar macrophages with concomitant activation of type II pneumocytes. In the terminal bronchioles a concentration-dependent increase of bromodeoxyuridine (BrdU)-labeled epithelial cells was observed in all PMDI exposure groups. In summary, it appears that respirable PMDI aerosol interacts with pulmonary surfactant, which, in turn, may stimulate type II pneumocytes to increase their production of surfactant and to proliferate.

Exposure to Microorganisms: Diseases and Diagnosis

Abstract The number of moisture-problem buildings in Finland is unexpectedly high according to recent investigations. In approximately 55% of Finnish buildings, moisture damage is in need of repair. With more than 1.15 million buildings in this country, almost 600 000 buildings suffer moisture problems and in over 100 000 there is growth of molds, either in building materials or on infested surfaces of the building. This means that over 400 000 Finns have been exposed to molds in damp houses. Exposure to molds is a significant health risk and should be prevented. Irritation of eyes, respiratory tract and skin may occur following exposure to microbes, and numbers of exposed persons develop a hypersensitivity reaction to fungal allergens. Asthma, hypersensitivity pneumonitis (extrinsic allergic alveolitis) and organic dust toxic syndrome (ODTS) may also develop after exposure. Secondary infections are more common in persons living in damp houses. In the present article, clinical manifestations associated with mold exposure in moisture-problem buildings will be described.

Airborne Mycotoxins in Agricultural and Indoor Environments

Abstract Mycotoxins are secondary metabolites produced by many species of fungi, such as Penicillium, Aspergillus, Fusarium and Stachybotrys. Mycotoxicosis can affect humans and animals after ingestion of mouldy, mycotoxin-contaminated food or feed. Recent years have seen increasing interest in inhalation exposure to mycotoxins in agricultural environments and in water-damaged buildings with mould problems. Inhalation exposure to mycotoxins can occur by inhalation of airborne mycotoxin-containing particles, such as fungal spores. There is evidence that inhalation exposure to aflatoxins can elevate cancer risk, and inhalation exposure to ochratoxins can cause kidney damage. In buildings with mould problems, trichothecene mycotoxins have been detected in building materials and dust samples. In these cases, residents have suffered from respiratory tract symptoms and irritation of eyes and skin.

Building-related illness and employee lost time following application of hot asphalt roof: a call for prevention.

Industrial hygiene sampling within an office building during and following a roof renovation revealed low-level exposure to high-boiling organic compounds, associated with complaints of eye and upper respiratory tract irritation among building occupants. Health complaints continued substantially beyond the time frame of the renovation completion, despite a lack of objective industrial hygiene findings for volatile organic compounds (VOCs) and microbiological contamination, and a lack of consistent medical findings among employees evaluated by an occupational physician. An analysis of employee attendance records suggests lost attendance and reduced productivity costs. Preventive strategies include proper planning and scheduling of building renovations to prevent employee exposure to asphalt roof emissions.

Twenty-eight-day repeated-dose inhalation exposure of rats to diethylene glycol monoethyl ether.

This study was carried out to provide information on the effects of inhalation of diethylene glycol monoethyl ether, a substance used in industry which may be accidentally inhaled by man. Sprague-Dawley CD rats were exposed by inhalation to a test atmosphere containing diethylene glycol monoethyl ether in a nose-only exposure system for 6 hr a day, 5 days a week for 28 days. Mean exposure levels were 0. 09, 0.27, and 1.1 mg/liter. At the two lowest exposure levels the test substance was present entirely as vapor, but at the highest exposure level the test atmosphere was approximately equally divided by mass into respirable droplets (aerosol) and vapor. A comprehensive battery of toxicological evaluations including food consumption, body weight, clinical signs, hematology, and biochemistry revealed no evidence of a systemic effect of exposure. Histopathological examination showed changes indicative of mild nonspecific irritation in the upper respiratory tract of rats exposed at the two highest exposure levels. These changes consisted of foci of necrosis in the ventral cartilage of the larynx of rats exposed at 0.27 or 1.1 mg/liter and an increase in eosinophilic inclusions in the olfactory epithelium of the nasal mucosa of rats exposed at 1.1 mg/liter. The no observed adverse effect level for systemic effects was 1.1 mg/liter and the no observed adverse effect level for signs indicative of mild nonspecific irritation of the upper respiratory tract was 0.09 mg/liter.