Work-related peak flow and asthma symptoms in a damp building.

BACKGROUND: Working in damp conditions is associated with asthma, but few studies have used objective testing to document work-related patterns. AIMS: To describe the relationship of peak flow measurements to work-related asthma (WRA) symptoms and WRA among occupants in a damp office building. METHODS: At the beginning of the study, all workers were offered a questionnaire and methacholine challenge testing. Participants were then instructed to perform serial spirometry using handheld spirometers five times per day over a 3 week period. Peak flow data were analysed using OASYS-2 software. We calculated the area between the curves (ABC score) using hours from waking. We considered a score >5.6 L/min/h to be indicative of a work-related pattern. RESULTS: All 24 employees participated in the questionnaire. Seven participants (29%) reported physician-diagnosed asthma with onset after starting work in the building. Almost two-thirds (63%) of participants reported at least one lower respiratory symptom (LRS) occurring one or more times per week in the last 4 weeks. Twenty-two (92%) consented to participate in serial spirometry. Fourteen participants had adequate quality of serial spirometry, five of whom had ABC scores >5.6, ranging from 5.9-23.0. Of these five, two had airways responsiveness, three had current post-hire onset physician-diagnosed asthma and four reported work-related LRS. CONCLUSIONS: We found evidence of work-related changes in serial peak flows among some occupants of an office building with a history of dampness. Serial peak flows may be a useful measure to determine WRA in office settings.

Lack of respiratory improvement following remediation of a water-damaged office building.

BACKGROUND: Damp buildings are commonly remediated without removing employees or ongoing medical surveillance. METHODS: We examined paired pulmonary function and questionnaire data from 2002 and 2005 for 97 employees in a water-damaged building during ongoing but incomplete remediation. RESULTS: We observed no overall improvement in respiratory health, as reflected in symptom scores, overall medication use, spirometry abnormalities, or sick leave. Four employees went from borderline bronchial hyperresponsiveness to bronchial hyperresponsiveness; six developed abnormal spirometry; three more reported post-occupancy current asthma, and four hypersensitivity pneumonitis. The number of participants without lower respiratory symptoms decreased from 27 in 2002 to 20 in 2005. Respiratory cases relocated in the building had a decrease in medication use and sick leave in 2005. CONCLUSIONS: During dampness remediation, relocation may be health protective and prevent incident building-related respiratory cases. Without relocation of entire workforces, medical surveillance is advisable for secondary prevention of existing building-related disease.

Symptoms after mould exposure including Stachybotrys chartarum, and comparison with darkroom disease.

BACKGROUND: Mould-attributed symptoms have included features which overlap with unexplained syndromes such as sick building syndrome. OBJECTIVES: We describe questionnaire and chart review findings in patients following exposure to moulds which include Stachybotrys and compare responses with two control groups. METHODS: Thirty-two patients presented with symptoms attributed to mould exposures. Exposure identification for 25 patients had reported S tachybotrys chartarum as well as other mould (Aspergillus, Penicillium), 88% at work. The remaining seven had professionally visualized or self-reported/photographic exposure evidence only. A chart review was performed and a follow-up with a questionnaire, including questions on current health status, and nonspecific symptoms. RESULTS: Cough, shortness of breath and chest tightness (at presentation) were reported in 79%, 70% and 64%, respectively, and persisted >6 weeks in 91%. Skin test(s) were positive to fungal extract(s) in 30%. Seventeen returned questionnaires were obtained 3.1 (SD 0.5) years after the initial clinic assessment. Among this subgroup, persisting asthma-like symptoms and symptoms suggestive of sick building syndrome were frequent, and similar to a group previously assessed for darkroom disease among medical radiation technologists. The mould-exposed group more commonly reported they were bothered when walking in a room with carpets, complained of a chemical or metallic taste in their mouth, and had problems in concentration when compared with a control physiotherapist group (P < 0.005). CONCLUSIONS: Although only a minority with health concerns from indoor mould exposure had demonstrable mould-allergy, a significant proportion had asthma-like symptoms. Other symptoms were also common and persistent after the initial implicated exposure.

Effects of green buildings on employee health and productivity.

We investigated the effects of improved indoor environmental quality (IEQ) on perceived health and productivity in occupants who moved from conventional to green (according to Leadership in Energy and Environmental Design ratings) office buildings. In 2 retrospective-prospective case studies we found that improved IEQ contributed to reductions in perceived absenteeism and work hours affected by asthma, respiratory allergies, depression, and stress and to self-reported improvements in productivity. These preliminary findings indicate that green buildings may positively affect public health.

Association between indoor exposure to semi-volatile organic compounds and building-related symptoms among the occupants of residential dwellings.

UNLABELLED: The aim of this study was to evaluate the levels of semi-volatile compounds (SVOCs) in residential detached houses in Sapporo, Japan, and whether exposure to these SVOCs was associated with the development of building-related symptoms named 'sick house syndrome' (SHS). The definition of SHS is fundamentally the same as that of the sick building syndrome (SBS). The presence of symptoms of SHS was evaluated using a validated self-administered questionnaire. Surveys and samplings of air and house dust in 41 dwellings were performed from October 2006 to January 2007, and 134 occupants responded to questionnaires. Samples were analyzed to quantify the concentrations of eight plasticizers, eleven phosphate triester flame retardants, two alkyl phenols used as anti-oxidants, and one organochlorine synergist called s-421, by gas chromatography-mass spectrometry and gas chromatography-flame photometry. The compounds frequently detected were di-n-butylphthalate, di(2-ethylhexyl)phthalate (DEHP), and dibutylhydroxytoluene in air, and DEHP and tris(2-butoxyethyl)phosphate (TBEP) in dust. Tributylphosphate was strongly and directly associated with mucosal symptoms of SHS; s-421 was also directly associated with mucosal symptoms of SHS. On the contrary, some chemicals such as diethylphthalate and TBEP were inversely associated with SHS. In future studies, we plan to assess these associations in a larger population. PRACTICAL IMPLICATIONS: This study suggests that it may be possible to reduce building-related symptoms by altering exposure to certain SVOCs, such as tributylphosphate commonly found in ceiling and wall coverings and s-421 used as a synergist for pyrethroids. The association between SHS and s-421 suggested that use of pyrethroid insecticides could elicit symptoms of SHS. However, further studies are necessary to test the associations observed in the present study and to examine whether the SVOCs associated with symptoms are causative agents or simply surrogates for some other factor that is causing the symptoms.

Indoor thermal factors and symptoms in office workers: findings from the US EPA BASE study.

UNLABELLED: Some prior research in office buildings has associated higher indoor temperatures even within the recommended thermal comfort range with increased worker symptoms. We reexamined this relationship in data from 95 office buildings in the US Environmental Protection Agency's Building Assessment Survey and Evaluation Study. We investigated relationships between building-related symptoms and thermal metrics constructed from real-time measurements. We estimated odds ratios and 95% confidence intervals in adjusted logistic regression models with general estimating equations, overall and by season. Winter indoor temperatures spanned the recommended winter comfort range; summer temperatures were mostly colder than the recommended summer range. Increasing indoor temperatures, overall, were associated with increases in few symptoms. Higher winter indoor temperatures, however, were associated with increases in all symptoms analyzed. Higher summer temperatures, above 23 degrees C, were associated with decreases in most symptoms. Humidity ratio, a metric of absolute humidity, showed few clear associations. Thus, increased symptoms with higher temperatures within the thermal comfort range were found only in winter. In summer, buildings were overcooled, and only the higher observed temperatures were within the comfort range; these were associated with decreased symptoms. Confirmation of these findings would suggest that thermal management guidelines consider health effects as well as comfort, and that less conditioning of buildings in both winter and summer may have unexpected health benefits. PRACTICAL IMPLICATIONS: In winter, higher temperatures within the thermal comfort range are common in US office buildings and may be associated with increased symptoms. In summer, temperatures below the thermal comfort range are common and may be associated with increased symptoms. Results from this large study thus suggest that in US office buildings, less winter heating (in buildings that are in heating mode) and less summer cooling may reduce acute symptoms while providing substantial energy conservation benefits, with no expected thermal comfort penalty and, in summer, even thermal comfort benefits. If confirmed, this would be welcome news.

Negative affect and chemical intolerance as risk factors for building-related symptoms: a controlled exposure study.

OBJECTIVE: To assess whether differences in negative affect (NA) and chemical intolerance (CI) affect responses to chemical mixtures and stress in a controlled experimental model. METHODS: Participants were 130 nonsmoking, healthy women, recruited from a university community. Participants completed the Positive and Negative Affect Scale and the Chemical Odor Intolerance Index. In separate sessions 1 week apart, they were exposed to volatile organic compounds (VOCs), VOCs with ozone (VOCs+O3), and ambient or filtered air with a 1-minute spike of VOCs (masked clean air). During each session, half of the participants performed a videotaped speech stressor and half performed simple arithmetic. Before, during, and after each session, salivary cortisol samples were collected, and subjects completed neurobehavioral tests and used a ratio scale to rate physical, cognitive, and anxiety symptoms. RESULTS: Relative to low NA or low CI, neither the high NA nor the high CI groups reported significantly more symptoms in response to any exposure condition. High NA subjects reported more anxiety symptoms in response to the speech stressor but did not have higher cortisol than low NA subjects. High NA subjects, however, were more distressed by the experimental conditions than were low NA subjects. Low NA subjects reported more severe anxiety in the VOCs+O3 with psychological stress condition. CONCLUSIONS: Subjects high in NA were more anxious after a stressor but were not more physically symptomatic in response to increasing chemical exposures. A disposition toward high or low CI did not result in a differential symptomatic response to controlled chemical exposures.

Symptoms, complaints, ocular and nasal physiological signs in university staff in relation to indoor environment - temperature and gender interactions.

UNLABELLED: Symptoms, signs, perceptions, and objective measures were studied in university buildings. Two problem buildings with a history of dampness and complaints were compared with two control buildings. Health investigations among university staff were performed at the workplace (n = 173) including tear film stability [non-invasive break-up time (NIBUT) and self-reported break-up time (SBUT)], nasal patency (acoustic rhinometry), nasal lavage fluid analysis [NAL: eosinophil cationic protein (ECP), myeloperoxidase (MPO), lysozyme and albumin] and atopy by total serum IgE and IgE antibodies (Phadiatop). Exposure assessment included inspections, thermal and atmospheric climate at 56 points modelled for all work sites. Multiple regressions were applied, controlling for age and gender. Exposure differences between problem buildings and controls were small, and variations between rooms were greater. Workers in the problem buildings had more general and dermal symptoms, but not more objective signs than the others. Adjusted day NIBUT and SBUT increased at higher night air temperatures, with B (95% CI) 0.6 (0.04-1.2) and 1.3 (-0.02 to 2.5), respectively. Higher relative humidity at mean day air temperature <22.1 degrees C was associated with adjusted NIBUT and SBUT, with B (95% CI) 0.16 (0.03-0.29) and 0.37 (-0.01 to 0.75), respectively. Air velocity below recommended winter values and reduced relative humidity in the range of 15-30% were associated with dry air and too low temperature. PRACTICAL IMPLICATIONS: Thermal climate in university buildings may be associated with both perceptions and physiological signs. Reduced night time air temperature, increased difference in air temperature between day and night, and fast changes in air temperature might impair indoor environment. This may have implication for energy-saving policies. It might be difficult to identify the exposure behind, and find the reason why, some buildings are defined as 'problem buildings'.

[Review of sick house syndrome].

'Sick house syndrome' (SHS) is a health issue that closely resembles sick building syndrome (SBS) that had occurred in European countries. The aim of this review is to clarify the characteristics of SHS by reviewing previous reports rigorously. We propose the definition of SHS as "health impairments caused by indoor air pollution, regardless of the place, causative substance, or pathogenesis". Cases of SBS are reported to occur predominantly in offices and sometimes schools, whereas those of SHS are usually found in general dwellings. In many cases, SHS is caused by biologically and/or chemically polluted indoor air. Physical factors might affect the impairments of SHS in some cases. It is considered that symptoms of SHS develop through toxic, allergic and/or some unknown mechanisms. Psychological mechanisms might also affect the development of SHS. It is still unclear whether SBS and SHS are very close or identical clinical entities, mostly because a general agreement on a diagnostic standard for SHS has not been established. Previous research gradually clarified the etiology of SHS. Further advances in research, diagnosis, and treatment of SHS are warranted with the following measures. Firstly, a clinical diagnostic standard including both subjective and objective findings must be established. Secondly, a standard procedure for assessing indoor air contamination should be established. Lastly, as previous research indicated multiple causative factors for SHS, an interdisciplinary approach is needed to obtain the grand picture of the syndrome.

Sick building syndrome (SBS) and exposure to water-damaged buildings: time series study, clinical trial and mechanisms.

Occupants of water-damaged buildings (WDBs) with evidence of microbial amplification often describe a syndrome involving multiple organ systems, commonly referred to as "sick building syndrome" (SBS), following chronic exposure to the indoor air. Studies have demonstrated that the indoor air of WDBs often contains a complex mixture of fungi, mycotoxins, bacteria, endotoxins, antigens, lipopolysaccharides, and biologically produced volatile compounds. A case-series study with medical assessments at five time points was conducted to characterize the syndrome after a double-blinded, placebo-controlled clinical trial conducted among a group of study participants investigated the efficacy of cholestyramine (CSM) therapy. The general hypothesis of the time series study was that chronic exposure to the indoor air of WDBs is associated with SBS. Consecutive clinical patients were screened for diagnosis of SBS using criteria of exposure potential, symptoms involving at least five organ systems, and the absence of confounding factors. Twenty-eight cases signed voluntary consent forms for participation in the time-series study and provided samples of microbial contaminants from water-damaged areas in the buildings they occupied. Twenty-six participants with a group-mean duration of illness of 11 months completed examinations at all five study time points. Thirteen of those participants also agreed to complete a double-blinded, placebo-controlled clinical trial. Data from Time Point 1 indicated a group-mean of 23 out of 37 symptoms evaluated; and visual contrast sensitivity (VCS), an indicator of neurological function, was abnormally low in all participants. Measurements of matrix metalloproteinase 9 (MMP9), leptin, alpha melanocyte stimulating hormone (MSH), vascular endothelial growth factor (VEGF), immunoglobulin E (IgE), and pulmonary function were abnormal in 22, 13, 25, 14, 1, and 7 participants, respectively. Following 2 weeks of CSM therapy to enhance toxin elimination rates, measurements at Time Point 2 indicated group-means of 4 symptoms with 65% improvement in VCS at mid-spatial frequency-both statistically significant improvements relative to Time Point 1. Moderate improvements were seen in MMP9, leptin, and VEGF serum levels. The improvements in health status were maintained at Time Point 3 following a 2-week period during which CSM therapy was suspended and the participants avoid re-exposure to the WDBs. Participants reoccupied the respective WDBs for 3 days without CSM therapy, and all participants reported relapse at Time Point 4. The group-mean number of symptoms increased from 4 at Time Point 2 to 15 and VCS at mid-spatial frequency declined by 42%, both statistically significant differences relative to Time Point 2. Statistically significant differences in the group-mean levels of MMP9 and leptin relative to Time Point 2 were also observed. CSM therapy was reinstated for 2 weeks prior to assessments at Time Point 5. Measurements at Time Point 5 indicated group-means of 3 symptoms and a 69% increase in VCS, both results statistically different from those at Time Points 1 and 4. Optically corrected Snellen Distance Equivalent visual acuity scores did not vary significantly over the course of the study. Group-mean levels of MMP9 and leptin showed statistically significant improvement at Time Point 5 relative to Time Points 1 and 4, and the proportion of participants with abnormal VEGF levels was significantly lower at Time Point 5 than at Time Point 1. The number of participants at Time Point 5 with abnormal levels of MMP9, leptin, VEGF, and pulmonary function were 10, 10, 9, and 7, respectively. The level of IgE was not re-measured because of the low incidence of abnormality at Time Point 1, and MSH was not re-measured because previously published data indicated a long time course for MSH improvement. The results from the time series study supported the general study hypothesis that exposure to the indoor air of WDBs is associated with SBS. High levels of MMP9 indicated that exposure to the complex mixture of substances in the indoor air of the WDBs triggered a pro-inflammatory cytokine response. A model describing modes of action along a pathway leading to biotoxin-associated illness is presented to organize current knowledge into testable hypotheses. The model links an inflammatory response with tissue hypoxia, as indicated by abnormal levels of VEGF, and disruption of the proopiomelanocortin pathway in the hypothalamus, as evidenced by abnormalities in leptin and MSH levels. Results from the clinical trial on CSM efficacy indicated highly significant improvement in group-mean number of symptoms and VCS scores relative to baseline in the 7 participants randomly assigned to receive 2 weeks of CSM therapy, but no improvement in the 6 participants assigned placebo therapy during that time interval. However, those 6 participants also showed a highly significant improvement in group-mean number of symptoms and VCS scores relative to baseline following a subsequent 2-week period of CSM therapy. Because the only known benefit of CSM therapy is to enhance the elimination rates of substances that accumulate in bile by preventing re-absorption during enterohepatic re-circulation, results from the clinical trial also supported the general study hypothesis that SBS is associated with exposure to WDBs because the only relevant function of CSM is to bind and remove toxigenic compounds. Only research that focuses on the signs, symptoms, and biochemical markers of patients with persistent illness following acute and/or chronic exposure to WDBs can further the development of the model describing modes of action in the biotoxin-associated pathway and guide the development of innovative and efficacious therapeutic interventions.

A case of sick building syndrome in a Japanese office worker.

The adverse health effects caused by indoor air pollution are termed "sick building syndrome". We report such a patient whose symptoms appeared in the workplace. A 36-year-old female office worker developed nausea and headache during working hours in a refurbished office. After eight months of seeking help at other clinics or hospitals without improvement, she was referred to our hospital. At that time she reacted to the smells of various chemicals outside of the office building. Biochemical findings were all within normal ranges. Specific IgE antibody to cedar pollen was positive and the ratio of TH1/TH2 was 4.5. In the Eye Tracking Test (ETT), vertical eye movement was saccadic. Her anxiety level was very high according to the State-Trait Anxiety Inventory (STAI) questionnaire. Subjective symptoms, ETT findings and anxiety levels on STAI gradually improved during two years of follow-up. One year after the onset of her illness, the formaldehyde concentrations in the building air ranged from 0.017-0.053 ppm. Even though relatively low, chemical exposure from building materials such as formaldehyde induced a range of symptoms. Also, lack of recognition by superiors and doctors that sick building syndrome might have been the source of her illness coupled with her high state of anxiety may have exacerbated her symptoms and led to the onset of multiple chemical sensitivity. Thus psychosocial factors may contribute to sick building syndrome in the workplace.

[Building related ilness]. / Enfermedades relacionadas con los edificios.

Following the changes carried out in recent years in buildings, such as ventilation systems, computers, etc., a series of diseases, that are related to this, have been described. This paper concentrates on the syndrome of the sick building, which is formed by a group of symptoms normally suffered by workers in the same "sick" building. This syndrome is related to its interior ambience, since the clinical manifestations appear some hours after entering the building and improves a few minutes after leaving this ambience. The origin is probably multifactorial: volatile airborne pollutants, the ventilation system, factors related to work organisation, or even dependent on the host. Since there is no single cause, we enumerate the risk factors in developing this syndrome as well as the steps for reaching a diagnosis and useful measures for preventing the sick building.

Indoor environmental exposures and symptoms.

The label "sick building syndrome" is often used to imply the absence of a physiologic basis for symptoms in the built environment. Although building-related illness is widely recognized but considered rare, several well-studied mechanisms may be responsible for many symptoms in buildings. These mechanisms do not explain why some individuals perceive disability. Until researchers distinguish physiologic mechanisms from other aspects of disease and study them systematically, poorly defined symptoms will remain poorly understood. The disability associated with such symptoms and syndromes, not the physiology, is the primary interest and generates controversy.

Environmental factors in medically unexplained symptoms and related syndromes: the evidence and the challenge.

Symptoms, and especially those without clear underlying medical explanations, account for a large percentage of clinical encounters. Many unexplained symptoms have been organized by patients and practitioners into syndromes such as chronic fatigue syndrome, multiple chemical sensitivity, sick building syndrome, Gulf War syndrome, and the like. All these syndromes are defined solely on the basis of symptoms rather than by medical signs. Some of the above-described conditions overlap strongly with explained conditions such as asthma. The relationship of such symptoms and syndromes to environmental exposure is often sharply debated, as is the distinction between the various syndromes. This leads to problems of what type of research should be conducted and who should conduct it. It is time to develop a comprehensive research agenda to sort out nomenclature, epidemiology, and environmental causation for these conditions, moving toward comprehensive and effective public health and clinical approaches.

The influence of sex, allergic rhinitis, and test system on nasal sensitivity to airborne irritants: a pilot study.

"Nasal irritant sensitivity" is an important construct in environmental health science; functional measures, however, lack standardization. We performed duplicate measures of nasal irritant perceptual acuity on 16 subjects (evenly divided by sex and seasonal allergy status) using two different test compounds: carbon dioxide (CO2) (detection) and n-propanol (localization). The a priori hypotheses included a) allergic rhinitics will display lower perceptual thresholds than nonrhinitics; b) females will display lower perceptual thresholds than males; and c) estimates of perceptual acuity using the two test systems will be positively correlated. We obtained CO2 detection thresholds using an ascending concentration series, presenting 3-sec pulses of CO2, paired with air in random order, by nasal cannula. We obtained localization thresholds by simultaneously presenting stimuli (ascending concentrations of n-propanol vapor in air) and blanks (saturated water vapor in air) to opposite nostrils, with laterality randomized. In terms of test-retest reliability, individual replicate measures for CO2 detection thresholds correlated more closely than did the localization thresholds of volatile organic compounds (VOC) (r = 0.65 and r = 0.60, respectively). As an intertest comparison, log-transformed individual mean CO2 and VOC measures were positively correlated with an r of 0.63 (p < 0.01). In univariate analyses, sex predicted both log-transformed CO2 and VOC thresholds (females being more "sensitive"; p < 0.05 and 0.001, respectively). Nasal allergies predicted sensory testing results only in the multivariate analysis, and then only for VOC localization (p < 0.05). The question of population variation in nasal irritant sensitivity (as well as the generalizability of results across test compounds) deserves further attention.

Pavlovian conditioning of emotional responses to olfactory and contextual stimuli: a potential model for the development and expression of chemical intolerance.

Chemical intolerance (CI) in humans is a poorly understood phenomenon of uncertain etiology, seemingly influenced by multiple factors both within and between affected individuals. Several authors have suggested that the development of CI in some individuals may be due, at least in part, to Pavlovian conditioning processes in which the expression of overt symptoms to certain substances reflects classically conditioned responses to previously neutral olfactory and contextual stimuli. In this paper, we describe the potential relationship between olfactory and contextual conditioning in experimental animals and the development and expression of CI in humans. Furthermore, as significant advances have been made in delineating the brain areas that underlie these learned responses, we also review recent research on the contributions of the amygdala and perirhinal cortical region to olfactory and contextual fear conditioning.

Sick building syndrome in like symptoms in emergency prefabricated accommodation.

The present study investigated the sources of discomfort and the symptoms reported by earthquake victims residing in temporary emergency prefabricated accommodation (prefab). The investigation was carried out by means of a questionnaire. 203 prefab occupants and 13 inhabitants of houses, who were chosen as reference population, replied in winter and 233 prefab occupants and 154 inhabitants of houses replied in summer. In both seasons more people living in prefabs indentified dry air, stuffy air, stale air, dust, dampness, uncomfortable temperature and bad odours as sources of discomfort. They also complained of general symptoms (headache, irritablility, insomnia, difficulty in concentration) and irritative symptoms of the eyes, upper and lower airways and skin. Multiple regression analysis identified the type of accommodation as the variable that most influenced the onset of general, ocular, upper and lower airway symptoms. Intrinsic characteristics of the prefabs (being constructed with synthetic materials, combustion sources, poor ventilation and insulation) and psychosocial factors e. losing their home, could have contributed to the onset of symptoms.

Indoor air effects after building renovation and in manufactured homes.

PROBLEM: The objective was to measure and compare the neurobehavioral and respiratory effects of exposures to indoor air in people living in manufactured homes and occupying buildings during renovation and compare them with effects on subjects exposed to formaldehyde at work. METHODS: Ten people living in manufactured homes and 10 people exposed to chemicals during renovation of their offices or homes had measurements made of balance, visual fields, reaction time, hearing, grip strength, and vibration sense. Psychological measurements included cognition, recall, perceptual motor speed, long-term memory, and mood states. RESULTS: Exposures to indoor air were associated with abnormal simple and choice reaction time, abnormal balance with the eyes open and with the eyes closed, abnormalities of color confusion index, scotoma in visual fields, reduced verbal recall, digit symbol score, and elevated abnormal moods. The effects on the two groups of 10 were similar and resembled those from formaldehyde exposure but with less cognitive impairment. CONCLUSIONS: Adverse effects from indoor air in manufactured homes and during renovations were less severe but similar to those from occupational formaldehyde exposures. This suggests that formaldehyde has a major role in health problems from indoor air.

Model development and research vision for the future of multiple chemical sensitivity.

Multiple chemical sensitivity (MCS) is characterized by heightened self-reported sensitivity to extremely low concentrations of chemicals. It has numerous symptoms in common with the sick building syndrome, the Gulf War syndrome, and chronic fatigue. Despite much research, reproducible objective findings are lacking for MCS, as is a sound model to explain it. This paper proposes a 2-step model combining the needed epidemiologic terminology with that of psychophysiological activation and sensitization. It is suggested that different environmental stressors act as initiators. After initiation, the limbic system and other parts of the brain become sensitized and hyperreactive to environmental triggers. Odor acts as one important trigger. Future research should use more biological assessments in combination with environmental and psychosocial data and involve patient groups with similar symptoms, although diagnosed as suffering from different entities. The similarities and differences of patients with such entities need to be understood before the entities themselves can be understood, diagnosed, treated, and prevented.

The vanilloid receptor as a putative target of diverse chemicals in multiple chemical sensitivity.

The vanilloid receptor (TRPV1 or VR1), widely distributed in the central and peripheral nervous system, is activated by a broad range of chemicals similar to those implicated in Multiple Chemical Sensitivity (MCS) Syndrome. The vanilloid receptor is reportedly hyperresponsive in MCS and can increase nitric oxide levels and stimulate N-methyl-D-aspartate (NMDA) receptor activity, both of which are important features in the previously proposed central role of nitric oxide and NMDA receptors in MCS. Vanilloid receptor activity is markedly altered by multiple mechanisms, possibly providing an explanation for the increased activity in MCS and symptom masking by previous chemical exposure. Activation of this receptor by certain mycotoxins may account for some cases of sick building syndrome, a frequent precursor of MCS. Twelve types of evidence implicate the vanilloid receptor as the major target of chemicals, including volatile organic solvents (but not pesticides) in MCS.