Measuring personal exposure to airborne mutagens and nicotine in environmental tobacco smoke

The exposure of individuals to environmental tobacco smoke (ETS) is of increasing public health concern because epidemiological studies have associated passive smoking with increased risk of a variety of adverse health effects among non-smokers including lung cancer. As a way to measure individual exposure to the mutagenic compounds in the complex mixture of ETS, we used a sensitive Salmonella/microsome micro pre-incubation (microsuspension) assay to detect mutagenicity of particulate matter collected on filters from low volume (1.7 1/min flow rate) personal sampling pumps. Airborne nicotine was collected concurrently as a marker for ETS exposure. In pilot-field studies, individual exposure to ETS was measured in two separate indoor environments in which smokers were present: a gambling casino and a bingo parlor. Total suspended particulate matter (TSP) was collected on filters worn near the breathing zone of non-smoking individuals. Sampling times ranged from 40 min to 6 h. All extracts of filters had detectable levels of mutagenic activity (TA98, +S9) resulting in airborne mutagenic activity concentrations of 500-5000 rev/m3. The mutagenic activity of the filters from the casino and bingo parlors was significantly correlated with total particulate matter per filters (n = 12; Rho = 0.85, p less than 0.01) and with airborne nicotine per filter (n = 12; Rho = 0.95, p less than 0.01). The microsuspension assay was sufficiently sensitive to detect the mutagens associated with extracts of particulate matter from low volume samples (0.2-0.6 m3) in these indoor environments over a relatively short sampling time, and could be useful in studies of personal exposure to the mutagens in environmental tobacco smoke. Further, airborne nicotine concentrations were highly correlated with airborne mutagenicity and the mutagenic activity associated with ETS could therefore be estimated by the concentrations of nicotine.     

The effect of coal stoves and environmental tobacco smoke on the level of urinary 1-hydroxypyrene

The objective of this study was to investigate a relationship between indoor air pollution from heating and cooking with coal-burning stoves and from environmental tobacco smoke (ETS), and the level of urinary 1-hydroxypyrene (1-OH-PY). 1-OH-PY was analysed in children living in three areas of Silesia, a province in Poland. Urine samples were collected in winter, (1) from children exposed to ETS and smoke resulting from indoor coal-burning and (2) from control children. Airborne particulates had been sampled by use of stationary samplers by the Regional Sanitary-Epidemiological Station, Katowice throughout 12 months prior to the urine sampling. The urinary level of 1-OH-PY tended to increase in children exposed to ETS, but the increase was not significant. The concentrations of 1-OH-PY in urine of passive smokers were significantly elevated only in Bytom where an index of smoking parents of the studied children was highest as compared to other areas. Exposure to polycyclic aromatic hydrocarbons (PAH) due to domestic heating and cooking with coal-burning stoves resulted in significantly increased levels of 1-OH-PY. The results of this study indicate that the uptake of PAH due to indoor air pollution strongly affected the level of 1-OH-PY and that the main source of PAH in indoor air was the household use of coal for heating and/or cooking. When the results associated with this kind of exposure were excluded, median 1-OH-PY levels from the three examined areas assumed a pattern more similar to that of the benzo(a)pyrene (BaP) concentrations in ambient air.     

Biological treatment of indoor air for VOC removal: potential and challenges

There is nowadays no single fully satisfactory method for VOC removal from indoor air due to the difficulties linked to the very low concentration (microg m(-3) range), diversity, and variability at which VOCs are typically found in the indoor environment. Although biological methods have shown a certain potential for this purpose, the specific characteristic of indoor air and the indoor air environment brings numerous challenges. In particular, new methods must be developed to inoculate, express, and maintain a suitable and diverse catabolic ability under conditions of trace substrate concentration which might not sustain microbial growth. In addition, the biological treatment of indoor air must be able to purify large amounts of air in confined environments with minimal nuisances and release of microorganisms. This requires technical innovations, the development of specific testing protocols and a deep understanding of microbial activities and the mechanisms of substrate uptake at trace concentrations.     

Practices contributing to biotic pollution in Air-conditioned indoor environments

Indoor environments play important roles in human health. The health hazards posed by polluted indoor environments include allergy, infections and toxicity. The term ‘sick building syndrome’ (SBS) describes causes of building occupants experiencing adverse health effects that appear to be linked to the time spent in a building. Questionnaire-based data were collected from the people who live or work in air-conditioned (A/C) rooms. Responses of the occupants were analyzed to understand the practices contributing to biotic pollution of indoor air-conditioned environments. Our survey revealed some interesting facts about the users of A/C rooms and their practices that may be contributing to the indoor air quality. The allergy complaints and use of anti-allergy medicines were noted commonly among the occupants of government (Govt.) organizations and computer training centers where cleaning of room and A/C filters were not done periodically. Cleaning practices may reduce the complaints.     

Environmental tobacco smoke and sudden infant death syndrome: a review

Environmental tobacco smoke (ETS), containing the developmental neurotoxicant, nicotine, is a prevalent component of indoor air pollution. Despite a strong association with active maternal smoking and sudden infant death syndrome (SIDS), information on the risk of SIDS due to prenatal and postnatal ETS exposure is relatively inconsistent. This literature review begins with a discussion and critique of existing epidemiologic data pertaining to ETS and SIDS. It then explores the biologic plausibility of this association, with comparison of the known association between active maternal smoking and SIDS, by examining metabolic and placental transfer issues associated with nicotine, and the biologic responses and mechanisms that may follow exposure to nicotine. Evidence indicates that prenatal and postnatal exposures to nicotine do occur from ETS exposure, but that the level of exposure is often substantially less than levels induced by active maternal smoking. Nicotine also has the capacity to concentrate in the fetus, regardless of exposure source. Experimental animal studies show that various doses of nicotine are capable of affecting a neonate's response to hypoxic conditions, a process thought to be related to SIDS outcomes. Mechanisms contributing to deficient hypoxia response include the ability of nicotine to act as a cholinergic stimulant through nicotinic acetylcholine receptor (nAChR) binding. The need for future research to investigate nicotine exposure and effects from non-maternal tobacco smoke sources in mid to late gestation is emphasized, along with a need to discourage smoking around both pregnant women and infants.     

The impact of plants on the reduction of volatile organic compounds in a small space

This study aims at examining the reduction of indoor air contaminants by plants placed in an indoor space. Field measurements were performed using Aglaonema brevispathum, Pachira aquatica, and Ficus benjamiana, which were verified as air-purifying plants by NASA. Three conditions for the amount of plants and positions were used in two separate rooms whose dimensions are identical. The concentration of Volatile Organic Compounds (VOCs) was monitored three hours after the plants were placed and three days after the plants were placed. The variations of concentration of Benzene, Toluene, Etylbenzene, and Xylene (BTEX), as well as Formaldehyde, which are all known as the major elements of Volatile Organic Compounds were monitored. The amount of reduction in concentration of Toluene and Formaldehyde was monitored 3 hours and 3 days after the plants were placed in the space. The reduction in the concentration of Benzene, Toluene, Etylbenzene, Xylene, and Formaldehyde was significantly greater when plants were present. When plants were placed near a window, the reduction of concentration was greater. The more plants were used, the more a reduction of indoor air contaminants occurred. The effect of reducing the concentration of air contaminants increased when the amount of plants increased, and when the plants were placed in sunny area. The concentration of Toluene was reduced by 45.6 microg/m(3) when 10% of the model space was occupied by Aglaonema brevispathum.     

Fungal pollution of indoor environments and its management

Indoor environments play important roles in human health. The health hazards posed by polluted indoor environments include allergy, infections and toxicity. Life style changes have resulted in a shift from open air environments to air tight, energy efficient, environments, in which people spend a substantial portion of their time. Most indoor air pollution comes from the hazardous non biological agents and biological agents. Fungi are ubiquitous in distribution and are a serious threat to public health in indoor environments. In this communication, we have reviewed the current status on biotic indoor air pollution, role of fungi as biological contaminants and their impact on human health.     

A genotoxic assessment of environmental tobacco smoke using bacterial bioassays

Recently, the National Research Council in the U.S.A. stated that laboratory studies of environmental tobacco smoke (ETS) should be important in identifying ETS carcinogens, their concentrations in typical daily environments, and in understanding how these compounds contribute to ETS dose-response relationships. This paper demonstrates that integrated chemical and bacterial mutagenicity information can be used to identify ETS genotoxicants, monitor human exposure, and make comparative assessments. Approximately 1/3 of the ETS constituents for which there is quantitative analytical chemistry information also have associated genotoxicity information. For example, 11 of the quantitated compounds are animal carcinogens. Work presented in this paper demonstrates that both the nonparticle-bound semivolatile and the particulate-bound organic material contain bacterial mutagens. These ETS organics give an equivalent of approximately 86,000 revertants per cigarette. In addition, this article summarized efforts to estimate ETS bacterial mutagenicity, to use bacterial tests for the monitoring of ETS-impacted indoor environments, and to use bacterial assays for the direct monitoring of human exposure.     

Genotoxicity of environmental tobacco smoke: a review

Environmental tobacco smoke (ETS), or second-hand smoke, is a widespread contaminant of indoor air in environments where smoking is not prohibited. It is a significant source of exposure to a large number of substances known to be hazardous to human health. Numerous expert panels have concluded that there is sufficient evidence to classify involuntary smoking (or passive smoking) as carcinogenic to humans. According to the recent evaluation by the International Agency for Research on Cancer, involuntary smoking causes lung cancer in never-smokers with an excess risk in the order of 20% for women and 30% for men. The present paper reviews studies on genotoxicity and related endpoints carried out on ETS since the mid-1980s. The evidence from in vitro studies demonstrates induction of DNA strand breaks, formation of DNA adducts, mutagenicity in bacterial assays and cytogenetic effects. In vivo experiments in rodents have shown that exposure to tobacco smoke, whole-body exposure to mainstream smoke (MS), sidestream smoke (SS), or their mixture, causes DNA single strand breaks, aromatic adducts and oxidative damage to DNA, chromosome aberrations and micronuclei. Genotoxicity of transplacental exposure to ETS has also been reported. Review of human biomarker studies conducted among non-smokers with involuntary exposure to tobacco smoke indicates presence of DNA adducts, urinary metabolites of carcinogens, urinary mutagenicity, SCEs and hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene mutations (in newborns exposed through involuntary smoking of the mother). Studies on human lung cancer from smokers and never-smokers involuntarily exposed to tobacco smoke suggest occurrence of similar kinds of genetic alterations in both groups. In conclusion, these overwhelming data are compatible with the current knowledge on the mechanisms of carcinogenesis of tobacco-related cancers, occurring not only in smokers but with a high biological plausibility also in involuntary smokers.     

Urinary mutagenicity in nonsmokers following exposure to fresh diluted sidestream cigarette smoke

Ten healthy male and 10 healthy female 'never-smoking' subjects (ages 21-50) participated in a 5-day environmental room study to determine if an acute exposure to a high level of fresh diluted sidestream smoke (FDSS) would alter urinary mutagenicity. On Monday, Tuesday, Thursday and Friday, the 20 subjects sat in environmental rooms for 7.33h and were exposed to filtered and humidified air. On Wednesday, the 20 subjects were exposed in the environmental rooms for 7.33h to an average respirable suspended particle (RSP) concentration of 179 microg/m(3) of FDSS generated by machine smoking 1R4F Kentucky reference cigarettes. This level of FDSS is approximately three times the ETS level seen in the top 5% of US workplaces which allow smoking. A cumulative 7.33h air sample from each environmental room was collected and determined to be mutagenic by Ames Salmonella assay. Subjects' urinary mutagenicity was measured on Wednesday as compared with Tuesday or Thursday by assaying concentrates of 24h urine samples in Ames Salmonella bacterial strains TA98 and YG1024. Diet was strictly controlled on all study days, with broiled and pan-fried meat not served to minimize ingestion of mutagenic protein pyrolysis products. Although all the urinary mutagenicity values were within the range reported for minor changes in diet, the subjects experienced a small but statistically significant increase (p<0.05) in urinary mutagenicity in strain YG1024, but not in the less sensitive strain TA98 on the day of FDSS exposure.     

Air pollutant effects on fetal and early postnatal development

Numerical research on the health effects of air pollution has been published in the last decade. Epidemiological studies have shown that children's exposure to air pollutants during fetal development and early postnatal life is associated with many types of health problems including abnormal development (low birth weight [LBW], very low birth weight [VLBW], preterm birth [PTB], intrauterine growth restriction [IUGR], congenital defects, and intrauterine and infant mortality), decreased lung growth, increased rates of respiratory tract infections, childhood asthma, behavioral problems, and neurocognitive decrements. This review focuses on the health effects of major outdoor air pollutants including particulates, carbon monoxide (CO), sulfur and nitrogen oxides (SO(2), NOx), ozone, and one common indoor air pollutant, environmental tobacco smoke (ETS). Animal data is presented that demonstrate perinatal windows of susceptibility to sidestream smoke, a surrogate for ETS, resulting in altered airway sensitivity and cell type frequency. A study of neonatal monkeys exposed to sidestream smoke during the perinatal period and/or early postnatal period that resulted in an altered balance of Th1-/Th2-cytokine secretion, skewing the immune response toward the allergy-associated Th2 cytokine phenotype, is also discussed.     

Biomonitoring of environmental tobacco smoke (ETS)-related exposure to 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)

The exposure of non-smokers to the tobacco-specific N-nitrosamine 4-(N-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a rodent lung carcinogen, was determined in the air of various indoor environments as well as by biomonitoring of non-smokers exposed to environmental tobacco smoke (ETS) under real-life conditions using the urinary NNK metabolites 4-(N-methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and [4-(N-methylnitrosamino)-1-(3-pyridyl)but-1-yl]-beta-O-D-glucosiduronic acid (NNAL-Gluc). NNK was not detectable (&lt;0.5 ng m^-3) in 11 rooms in which smoking did not occur. The mean NNK concentration in 19 rooms in which smoking took place was 17.5 (2.4-50.0) ng m^-3. The NNK levels significantly correlated with the nicotine levels (r=0.856; p&lt; 0.0001). Of the 29 non-smokers investigated, 12 exhibited no detectable NNAL and NNAL-Gluc excretion (&lt;3 pmol day) in their urine. The mean urinary excretion of NNAL and NNAL-Gluc of the 17 remaining non-smokers was 20.3 (&lt;3-63.2) and 22.9 (&lt;3-90.0) pmol day^-1, respectively. Total NNAL excretion (NNAL+NNAL-Gluc) in all non-smokers investigated significantly correlated with the amount of nicotine on personal samplers worn during the week prior to urine collection (r=0.88; &lt;0.0001) and with the urinary cotinine levels (r=0.40; p=0.038). No correlation was found between NNAL excretion and the reported extent of ETS exposure. Average total NNAL excretion in the non-smokers with detectable NNAL levels was 74 times less than in 20 smokers who were also investigated. The cotinine/total NNAL ratios in urine of smokers (9900) and non-smokers (9300) were similar. This appears to be at variance with the ratios of the corresponding precursors (nicotine/NNK) in mainstream smoke (16400) and ETS (1000). Possible reasons for this discrepancy are discussed. The possible role of NNK as a lung carcinogen in non-smokers is unclear, especially since NNK exposure in non-smokers is several orders of magnitude lower than the ordinary exposure to exogenous and endogenous N-nitrosamines and the role of NNK as a human lung carcinogen is not fully understood.     

Human cancer from environmental pollutants: the epidemiological evidence

An increased risk of mesothelioma has been reported among individuals experiencing residential exposure to asbestos, while results for lung cancer are less consistent. Several studies have reported an increased risk of lung cancer risk from outdoor air pollution: on the basis of the results of the largest study, the proportion of lung cancers attributable to urban air pollution in Europe can be as high as 10.7%. A causal association has been established between second-hand tobacco smoking and lung cancer, which may be responsible for 1.6% of lung cancers. Radon is another carcinogen present in indoor air, which may be responsible for 4.5% of lung cancers. An increased risk of bladder might be due to water chlorination by-products. The available evidence on cancer risk following exposure to other environmental pollutants, including, pesticides, dioxins and electro-magnetic fields, is inconclusive.     

Indoor sources of mutagenic aerosol particulate matter: smoking, cooking and incense burning

The emission of aerosol particles and their mutagenic activity as well as the emission of some gaseous pollutants has been studied experimentally in order to compare the emission from some indoor pyrolysis processes. Cigarette (tobacco and herbal) smoking, incense and mosquito-coil burning and frying of experimental lean minced pork emitted particulate matter. Their extracts were mutagenic in the Ames Salmonella test with TA98 and activation as well as, with a higher response, in a microsuspension test with the same strain and activation condition. The response of the particles from the smoking and burning processes varied from 3000 to 50,000 revertants per gram of smoked or burnt material in the conventional Salmonella test and from 50,000 to 350,000 revertants per gram in the microsuspension assay. The frying of lean minced pork gave an airborne emission of about 53 and 560 revertants per gram of fried pork, respectively, in the 2 assays. The frying of some common food items following cookbook recipes also emitted mutagenic aerosol particles but the emitted activity was less than that in the pork experiment. Carbon monoxide, isoprene and benzene were present in the emissions from the smoking and burning processes but were not detectable in the frying fumes. The results suggest that incense and mosquito-coil burning can cause indoor air pollution akin to that from cigarette smoking. Indoor air pollution from cooking requires further study.     

Genotoxicity and PAC analysis of particulate and vapour phases of environmental tobacco smoke

Samples of indoor air were collected from an office room (88 m3) both before smoking and during experimental smoking of 96 cigarettes by 10 persons within 6 h. The particulates were collected on glass-fibre filters and the vapour-phase compounds on XAD-2 resin. The samples were extracted with acetone and analysed quantitatively for polycyclic aromatic compounds and qualitatively with GC-MS. The extracts of filters and XAD-2 resins were fractionated into neutral/acidic and 2 basic (strong and weak bases) fractions; all these fractions were tested with the sister-chromatid exchange (SCE) assay in Chinese hamster ovary (CHO) cells and with the Salmonella/microsome test (strain TA98). Total concentrations of PAC were 205 ng/m3 in the background sample and 1207 ng/m3 after contamination by cigarette smoking. The total PAC concentrations were 4-6 times higher in the vapour phase than in the particulate phase. The fractions of the particulate samples collected before smoking showed mainly marginal genotoxic activity, whereas after smoking their genotoxicity increased dramatically. The fractions of the vapour phase samples were not genotoxic before smoking, but after smoking the neutral/acidic and strong basic fractions induced responses in both assays. The SCE assay was more sensitive towards the vapour-phase mutagens of environmental tobacco smoke (ETS). The relative responses of the two basic fractions, whereas the fraction containing neutral and acidic compounds was the most potent in the SCE assay. In the Salmonella test, the mutagenic activity was mainly detected with metabolic activation, while the induction of SCE in CHO cells was also seen without an exogenous metabolic activation system.     

Mutagenicity and carcinogenicity of tea, Camellia sinensis

Aqueous, caffeine free and tannin fractions of commercial tea and tannic acid were tested for mutagenicity in Ames test. Tea fractions of tannic acid were non mutagenic in strains TA 100, TA 98, TA 1535 and TA 1538 of Salmonella typhimurium with or without metabolic activation (rat-S9 mix) at different doses tested. In strain TA 98 the above tea fractions and tannic acid inhibited the S9 mix mediated mutagenicity of tobacco in a dose dependent manner. The different tea fractions at 60 degrees C, did not increase the tumor incidence in Swiss mice by gavage feeding. They also failed to produce tumors when injected subcutaneously. Caffeine free tea extract decreased the tobacco induced liver tumors but had no effect on lung tumors. The same fraction was ineffective in hexachlorocyclohexane induced liver tumors in Swiss mice.     

Non-cancer effects of chemical agents on children's health

This paper provides an overview about the non-cancer health effects for children from relevant chemical agents in our environment. In addition, a meta-analysis was conducted on the association between sudden infant death syndrome (SIDS) and maternal smoking during pregnancy as well as postnatal exposure to environmental tobacco smoke (ETS).In children, birth deformities, neurodevelopment, reproductive outcomes and respiratory system are mainly affected by chemical exposures. According to recent systematic reviews, evidence is sufficient for cognitive impairments caused by low lead exposure levels. Evidence for neurotoxicity from prenatal methylmercury exposure is sufficient for high exposure levels and limited for low levels. Prenatal exposure to polychlorinated biphenyls (PCB) and related toxicants results in cognitive and motor deficits.Maternal smoking during pregnancy is a risk factor for preterm birth, foetal growth deficit and SIDS. The meta-analytic pooled risk estimate for SIDS based on 15 studies is 2.94 (95% confidence interval: 2.43–3.57). Postnatal exposure to ETS was found to increase the SIDS risk by a factor of 1.72 (95% CI: 1.28–2.30) based on six studies which took into account maternal smoking during pregnancy. Additionally, postnatal ETS exposure causes acute respiratory infections, ear problems, respiratory symptoms, more severe asthma, and it slows lung growth. These health effects are also of concern for postnatal exposure to ambient and indoor air pollution.Children differ from adults with respect to several aspects which are relevant for assessing their health risk. Thus, independent evaluation of toxicity in childhood populations is essential.     

Deaths and Medical Visits Attributable to Environmental Pollution in the United Arab Emirates

Background

This study estimates the potential health gains achievable in the United Arab Emirates (UAE) with improved controls on environmental pollution. The UAE is an emerging economy in which population health risks have shifted rapidly from infectious diseases to chronic conditions observed in developed nations. The UAE government commissioned this work as part of an environmental health strategic planning project intended to address this shift in the nature of the country’s disease burden.

Methods and Findings

We assessed the burden of disease attributable to six environmental exposure routes outdoor air, indoor air, drinking water, coastal water, occupational environments, and climate change. For every exposure route, we integrated UAE environmental monitoring and public health data in a spatially resolved Monte Carlo simulation model to estimate the annual disease burden attributable to selected pollutants. The assessment included the entire UAE population (4.5 million for the year of analysis). The study found that outdoor air pollution was the leading contributor to mortality, with 651 attributable deaths (95% confidence interval [CI] 143–1,440), or 7.3% of all deaths. Indoor air pollution and occupational exposures were the second and third leading contributors to mortality, with 153 (95% CI 85–216) and 46 attributable deaths (95% CI 26–72), respectively. The leading contributor to health-care facility visits was drinking water pollution, to which 46,600 (95% CI 15,300–61,400) health-care facility visits were attributed (about 15% of the visits for all the diseases considered in this study). Major study limitations included (1) a lack of information needed to translate health-care facility visits to quality-adjusted-life-year estimates and (2) insufficient spatial coverage of environmental data.

Conclusions

Based on international comparisons, the UAE’s environmental disease burden is low for all factors except outdoor air pollution. From a public health perspective, reducing pollutant emissions to outdoor air should be a high priority for the UAE’s environmental agencies.     

Recent advances in biological systems for improving indoor air quality

Reviews in Environmental Science and Bio/Technology - Studies on human exposure to indoor air pollution reveal that indoor environments could be at least twice as polluted as outdoor environments....     

Detection of airborne Stachybotrys chartarum macrocyclic trichothecene mycotoxins in the indoor environment

The existence of airborne mycotoxins in mold-contaminated buildings has long been hypothesized to be a potential occupant health risk. However, little work has been done to demonstrate the presence of these compounds in such environments. The presence of airborne macrocyclic trichothecene mycotoxins in indoor environments with known Stachybotrys chartarum contamination was therefore investigated. In seven buildings, air was collected using a high-volume liquid impaction bioaerosol sampler (SpinCon PAS 450-10) under static or disturbed conditions. An additional building was sampled using an Andersen GPS-1 PUF sampler modified to separate and collect particulates smaller than conidia. Four control buildings (i.e., no detectable S. chartarum growth or history of water damage) and outdoor air were also tested. Samples were analyzed using a macrocyclic trichothecene-specific enzyme-linked immunosorbent assay (ELISA). ELISA specificity was tested using phosphate-buffered saline extracts of the fungal genera Aspergillus, Chaetomium, Cladosporium, Fusarium, Memnoniella, Penicillium, Rhizopus, and Trichoderma, five Stachybotrys strains, and the indoor air allergens Can f 1, Der p 1, and Fel d 1. For test buildings, the results showed that detectable toxin concentrations increased with the sampling time and short periods of air disturbance. Trichothecene values ranged from <10 to >1,300 pg/m3 of sampled air. The control environments demonstrated statistically significantly (P < 0.001) lower levels of airborne trichothecenes. ELISA specificity experiments demonstrated a high specificity for the trichothecene-producing strain of S. chartarum. Our data indicate that airborne macrocyclic trichothecenes can exist in Stachybotrys-contaminated buildings, and this should be taken into consideration in future indoor air quality investigations.