Low serum high-density lipoprotein cholesterol in childhood is associated with adolescent asthma.

BACKGROUND: Whilst emerging evidence from animal and cell experiments has shown high-density lipoprotein cholesterol to have anti-inflammatory effects consistent with a protective role in asthma, human studies investigating the relationship of high-density lipoprotein cholesterol with asthma have produced conflicting results. OBJECTIVE: To examine the association between serum lipids among Cypriot children aged 11-12 years and prevalence of asthma at age 15-17 years. METHODS: In 3982 children, we assessed serum lipids, body mass index and maximal oxygen consumption at baseline (2001-2003) and explored associations with respiratory health at follow-up (2007) using multiple logistic regression models. RESULTS: Lower levels of high-density lipoprotein cholesterol at age 11-12 years were found in subjects who reported ever asthma (58.2 vs. 60.0 mg/dL, P = 0.005) and active asthma (57.5 vs. 59.9 mg/dL, P = 0.010) in adolescence, in comparison with their respective reference groups. Total cholesterol, low-density lipoprotein and triglycerides had no association with any of the asthma outcomes. In contrast, with estimated odds ratios of 1.89 (95% CI 1.19-3.00) and 1.89 (95% CI 1.02-3.53), ever asthma and active asthma respectively appeared particularly pronounced among those who at baseline had high-density lipoprotein cholesterol <40 mg/dL, even after adjusting for potential confounders including body mass index and maximal oxygen consumption. CONCLUSIONS & CLINICAL RELEVANCE: Low-serum high-density lipoprotein cholesterol in childhood is associated with an increased risk for asthma in adolescence, suggesting a potential role of this lipoprotein in the pathogenesis of paediatric asthma.

Multiple microbial exposures in the home may protect against asthma or allergy in childhood.

BACKGROUND: Experimental animal data on the gram-negative bacterial (GNB) biomarker endotoxin suggest that persistence, dose, and timing of exposure are likely to influence its effects on allergy and wheeze. In epidemiologic studies, endotoxin may be a sentinel marker for a microbial milieu, including gram-positive bacteria (GPB) as well as GNB, that may influence allergy and asthma through components (pathogen-associated molecular patterns) that signal through innate Toll-like receptor pathways. OBJECTIVE: To determine the influence of current GNB and GPB exposures on asthma and allergic sensitization in school-aged children. METHODS: We examined the relationship between bacterial biomarkers and current asthma and allergic sensitization in 377 school-aged children in a birth cohort study. We then evaluated the effects of school-aged endotoxin, after controlling for exposure in early life. RESULTS: Exposure to GNB was inversely associated with asthma and allergic sensitization at school age [for >median endotoxin: prevalence odds ratio (POR)=0.34, 95% CI=0.2-0.7, for current asthma and prevalence ratio=0.77, 95% CI=0.6-0.97, for allergic sensitization]. In contrast, elevated GPB in the bed was inversely associated with current asthma (POR=0.41, 95% CI=0.2-0.9) but not with allergic sensitization (POR=1.07, 95% CI=0.8-1.4). School-aged endotoxin exposure remained protective in models for allergic disease adjusted for early-life endotoxin. CONCLUSION: Both GNB and GPB exposures are associated with decreased asthma symptoms, but may act through different mechanisms to confer protection. Endotoxin exposure in later childhood is not simply a surrogate of early-life exposure; it has independent protective effects on allergic disease.

Airborne influenza virus detection with four aerosol samplers using molecular and infectivity assays: considerations for a new infectious virus aerosol sampler.

As a first step in conducting studies of airborne influenza transmission, we compared the collection performance of an SKC Biosampler, a compact cascade impactor (CCI), Teflon filters, and gelatin filters by collecting aerosolized influenza virus in a one-pass aerosol chamber. Influenza virus infectivity was determined using a fluorescent focus assay and influenza virus nucleic acid (originating from viable and non-viable viruses) was measured using quantitative PCR. The results showed that the SKC Biosampler recovered and preserved influenza virus infectivity much better than the other samplers - the CCI, Teflon, and gelatin filters recovered only 7-22% of infectious viruses compared with the Biosampler. Total virus collection was not significantly different among the SKC Biosampler, the gelatin, and Teflon filters, but was significantly lower in the CCI. Results from this study show that a new sampler is needed for virus aerosol sampling, as commercially available samplers do not efficiently collect and conserve virus infectivity. Applications for a new sampler include studies of airborne disease transmission and bioterrorism monitoring. Design parameters for a new sampler include high collection efficiency for fine particles and liquid sampling media to preserve infectivity. Practical Implications New air samplers are needed to study infectious airborne viruses and learn about airborne disease transmission. As a first step in designing a new air sampler to collect influenza virus we evaluated four commercial samplers and determined necessary design parameters for a new collector.

Evaluating building-related symptoms using the US EPA BASE study results.

UNLABELLED: In order to develop baseline data about United States office buildings, the United States Environmental Protection Agency conducted the Building Assessment Survey Evaluation (BASE) study, a systematic survey of 100 randomly selected United States office buildings, in the 1990s. This paper analyzes the self-reported work-related symptoms and job and workplace characteristics of 4326 respondents and compares results to the National Institute for Occupational Safety and Health's (NIOSH) study of 80 'complaint' buildings. Four distinct groups of symptoms, representing 'tiredness', 'mucosal irritation', 'neuropsychological', and 'lower respiratory' conditions emerged from factor analysis of work-related symptoms. The symptom grouping is identical for both surveys. Although the prevalence of each symptom is significantly higher in the NIOSH than in the BASE sample, there is overlap of the symptom distributions. In the BASE survey, 45% of the work force reported at least one work-related health symptom; 20% reported at least three symptoms. These findings imply that it is counterproductive to dichotomize buildings into healthy vs. unhealthy; instead the prevalence of health problems related to buildings span a continuum. PRACTICAL IMPLICATIONS: These results indicate that most office buildings have occupants who report building-related symptoms. This paper provides practical guidance for the comparison of building prevalences to the BASE normative data. Work-related symptom distributions and symptom groups can improve investigators' ability to identify IEQ problems.

The frequency of workplace exacerbation among health maintenance organisation members with asthma.

OBJECTIVES: Workplace conditions can potentially contribute to the worsening of asthma, yet it is unclear what percentage of adults with asthma experience workplace exacerbation of symptoms. The objective of this investigation was to determine the prevalence of workplace exacerbation of asthma (WEA). METHODS: Adults with asthma aged 18-44 were enrolled into the baseline survey of a longitudinal study. Members of a health maintenance organisation were considered candidates for participation if they fulfilled membership, diagnostic, and treatment criteria based on automated review of electronic billing, claims, and pharmacy records. Diagnosis and treatment were confirmed by manual review of medical records. A telephone questionnaire was administered. A work related symptom score was assigned to each participant based on responses to questions about work related asthma symptoms, medication use, and symptom triggers. Blinded to participants' answers to these questions, two researchers independently reviewed the self-reported work histories and assigned exposure ratings. A final exposure score was then calculated. Participants with sufficient evidence for work related symptoms and exposure were classified as having WEA. RESULTS: Of the 598 participants with complete data, 557 (93%) were working, and 136 (23%) fulfilled the criteria for WEA. Those with WEA were more likely to be male and to report that they had been bothered by asthma symptoms during the past seven days. CONCLUSIONS: Workplace exacerbation of asthma was common in this study population, occurring in over a fifth of these adults with asthma. Physicians should consider that work can contribute to the exacerbation of symptoms when treating adults with asthma.

Risk of indoor airborne infection transmission estimated from carbon dioxide concentration.

The Wells-Riley equation, which is used to model the risk of indoor airborne transmission of infectious diseases such as tuberculosis, is sometimes problematic because it assumes steady-state conditions and requires measurement of outdoor air supply rates, which are frequently difficult to measure and often vary with time. We derive an alternative equation that avoids these problems by determining the fraction of inhaled air that has been exhaled previously by someone in the building (rebreathed fraction) using CO2 concentration as a marker for exhaled-breath exposure. We also derive a non-steady-state version of the Wells-Riley equation which is especially useful in poorly ventilated environments when outdoor air supply rates can be assumed constant. Finally, we derive the relationship between the average number of secondary cases infected by each primary case in a building and exposure to exhaled breath and demonstrate that there is likely to be an achievable critical rebreathed fraction of indoor air below which airborne propagation of common respiratory infections and influenza will not occur.

Characterization of endotoxin and 3-hydroxy fatty acid levels in air and settled dust from commercial aircraft cabins.

Endotoxin was measured in air and dust samples collected during four commercial aircraft flights. Samples were analyzed for endotoxin biological activity using the Limulus assay. 3-hydroxy fatty acids (3-OH FA) of carbon chain lengths C10:0-C18:0 were determined in dust by gas chromatography-ion trap tandem mass spectrometry. The geometric mean (geometric standard deviation) endotoxin air level was 1.5 EU/m3 (1.9, n = 28); however, significant differences were found by flight within aircraft type. Mean endotoxin levels were significantly higher in carpet dust than in seat dust (140 +/- 81 vs. 51 +/- 25 EU/mg dust, n = 32 each, P < 0.001). Airborne endotoxin levels were not significantly related to either carpet or seat dust endotoxin levels. Mean 3-OH FA levels were significantly higher in carpet dust than in seat dust for C10:2, C12:0, and C14:0 (P < 0.001 for each), while the mean level of C16:0 was significantly higher in seat dust than in carpet dust (P < 0.01). Carpet dust endotoxin was significantly, but moderately, correlated with 3-OH-C12:0 and 3-OH-C14:0 (Pearson r = 0.52 and 0.48, respectively), while correlation of seat dust endotoxin with individual 3-OH FAs depended on the test statistic used. Mean endotoxin potency was significantly higher for carpet dust than for seat dust (6.3 +/- 3.0 vs. 3.0 +/- 1.4 EU/pmol LPS, P < 0.0001). Mean endotoxin levels in the air and dust of commercial aircraft cabins were generally higher than mean levels reported in homes and office buildings. These results suggest that exposure route and dust source are important considerations when relating endotoxin exposure to specific health outcomes.

Enzyme-linked immunosorbent assay specific for (1-->6) branched, (1-->3)-beta-D-glucan detection in environmental samples.

(1-->3)-beta-D-Glucans have been recognized as a potential causative agent responsible for bioaerosol-induced respiratory symptoms observed in both indoor and occupational environments. A specific enzyme immunoassay was developed to quantify (1-->6) branched, (1-->3)-beta-D-glucans in environmental samples. The assay was based on the use of a high-affinity receptor (galactosyl ceramide) specific for (1-->3)-beta-D-glucans as a capture reagent and a monoclonal antibody specific for fungal cell wall beta-D-glucans as a detector reagent. The assay was highly specific for (1-->6) branched, (1-->3)-beta-D-glucans (such as that from Saccharomyces cerevisiae) and did not show any response at 200 ng/ml to curdlan, laminarin, pustulan, dextran, mannan, carboxymethyl cellulose, and endotoxins. The detection level was 0.8 ng/ml for baker's yeast glucan and Betafectin. A coefficient of variation of 7.8% was obtained for (1-->3)-beta-D-glucans in house dust samples. Metal working fluids spiked with (1-->3)-beta-D-glucans inhibited the glucan assay. Because the assay is specific for (1-->6) branched, (1-->3)-beta-D-glucans and is sensitive and reproducible, it will be useful for the investigation of health effects from exposure to this class of biologically active molecules.

Predictors of airborne endotoxin in the home.

We identified home characteristics associated with the level of airborne endotoxin in 111 Boston-area homes enrolled in a cohort study of home exposures and childhood asthma, and we developed a predictive model to estimate airborne endotoxin. We measured endotoxin in family-room air and in dust from the baby's bed, family room, bedroom, and kitchen floor. Level of airborne endotoxin was weakly correlated (r < 0.3) with level of endotoxin in each of the four types of dust samples and was significantly correlated with endotoxin in family-room dust (p < 0.05). Endotoxin in family-room dust accounted for < 6% of the variability of airborne endotoxin. In a multivariate model, certain home characteristics were positively (p < 0.05) associated with airborne endotoxin. These included current presence of dog (difference in level, dog vs. no dog = 72%, partial R(2 )= 12.8%), past presence of dog (partial R(2) = 5.5%), and endotoxin level in family-room dust (partial R(2) = 5.3%). Use of a dehumidifier (partial R(2) = 6.4%) was negatively associated (p = 0.02; difference = -31%) with airborne endotoxin. Other home characteristics were identified as important determinants of increased airborne endotoxin in this model, but individual coefficients were not statistically significant (alpha = 0.05): total amount of fine dust collected in the home (partial R(2 )= 3.8%), concrete floor in family room (3.7%), water damage (3.6%), and use of cool-mist humidifier in past year (2.7%). This multivariate model explained 42% of the variability of airborne endotoxin levels, a substantial improvement over that with dust endotoxin alone. Airborne endotoxin in Boston-area homes appears to be determined by the presence of dogs, moisture sources, and increased amounts of settled dust.

Endotoxin-stimulated innate immunity: A contributing factor for asthma.

Exposure to airborne endotoxin in infancy may protect against asthma by promoting enhanced T(H)1 response and tolerance to allergens. On the other hand, later in life, it adversely affects patients with asthma. Endotoxin binding to receptors on macrophages and other cells generates IL-12, which inhibits IgE responses. It also generates cytokines like IL-1, TNF-alpha, and IL-8, which cause inflammation. These signal transduction pathways resemble those leading to the generation of cytokines, such as IL-4, IL-13, and IL-5, which are responsible for the inflammation of IgE-mediated allergic disease. The main difference seems to be that endotoxin recruits neutrophils, but IgE recruits eosinophils, and the details of the tissue injury from these granulocytes differ. Sources of airborne endotoxin include many agricultural dusts, aerosols from contaminated water in many industrial plants, contaminated heating and air-conditioning systems, mist-generating humidifiers, and damp or water-damaged homes. Acute inhalation of high concentrations of endotoxin can cause fever, cough, and dyspnea. Chronic inhalation of lesser amounts causes chronic bronchitis and emphysema and is associated with airway hyperresponsiveness. Airborne endotoxin adversely affects patients with asthma in 3 ways: (1) by increasing the severity of the airway inflammation; (2) by increasing the susceptibility to rhinovirus-induced colds; and (3) by causing chronic bronchitis and emphysema with development of irreversible airway obstruction after chronic exposure of adults. The most effective management is mitigating exposure. The potential of drug treatments requires further clinical investigation.

House dust endotoxin and wheeze in the first year of life.

We examined endotoxin exposure and wheezing episodes during the first year of life in a birth cohort of 499 infants with one or both parents having a history of asthma or allergy. We measured endotoxin in settled dust from the baby's bed, bedroom floor, family room, and kitchen floor within the first 3 mo after birth. The primary outcomes were any wheeze (versus no wheeze), and repeated wheeze (versus one or no report of wheeze). We found a significant univariate association of elevated endotoxin (> or = 100 EU/ mg) in family room dust with increased risk of any wheeze (Relative Risk = 1.29, 95% CI = 1.03-1.62). The association was not confounded by cockroach allergen, lower respiratory illness (croup, bronchitis, bronchiolitis, and pneumonia), smoking during pregnancy, lower birth weight, maternal asthma, presence of dog, and race/ethnicity in a multivariate model; the multivariate relative risk (RR = 1.33) was marginally significant (95% CI: 1.00-1.76, p < 0.05). In a multivariate model, controlling for the above covariates, elevated endotoxin in family room dust was significantly associated with increased risk (RR = 1.56, 95% CI = 1.03-2.38) of repeated wheeze. These results suggest that home endotoxin exposure may independently increase risk of any wheeze and repeated wheeze during the first year of life for children with a familial predisposition to asthma or allergy.

Longitudinal study of dust and airborne endotoxin in the home.

To characterize the seasonal variability of endotoxin levels, we measured endotoxin in dust from the bed, bedroom floor, and kitchen floor in 20 homes, and in air from the bedroom in 15 of the homes. All homes were located in the greater Boston, Massachusetts, area and were sampled each month from April 1995 to June 1996. Outdoor air was collected at two locations. We found greater within-home than between-home variance for bedroom floor, kitchen floor, and airborne endotoxin. However, the reverse was true for bed dust endotoxin. Thus, studies using single measurements of dust endotoxin are most likely to reliably distinguish between homes if bed dust is sampled. Dust endotoxin levels were not significantly associated with airborne endotoxin. Airborne endotoxin was significantly (p = 0. 04) and positively associated with absolute humidity in a mixed-effect model adjusting for a random home effect and fixed effect of sampling month and home characteristics. This finding implies that indoor humidity may be an important factor controlling endotoxin exposure. We found a significant (p < 0.05) seasonal effect in kitchen floor dust (spring > fall) and bedroom airborne endotoxin (spring > winter), but not in the other indoor samples. We found significant seasonal pattern in outdoor airborne endotoxin (summer > winter).

Risk of sick leave associated with outdoor air supply rate, humidification, and occupant complaints.

We analyzed 1994 sick leave for 3,720 hourly employees of a large Massachusetts manufacturer, in 40 buildings with 115 independently ventilated work areas. Corporate records identified building characteristics and IEQ complaints. We rated ventilation as moderate (approximately 25 cfm/person, 12 ls-1) or high (approximately 50 cfm/person, 24 ls-1) outdoor air supply based on knowledge of ventilation systems and CO2 measurements on a subset of work areas, and used Poisson regression to analyze sick leave controlled for age, gender, seniority, hours of non-illness absence, shift, ethnicity, crowding, and type of job (office, technical, or manufacturing worker). We found consistent associations of increased sick leave with lower levels of outdoor air supply and IEQ complaints. Among office workers, the relative risk for short-term sick leave was 1.53 (95% confidence 1.22-1.92) with lower ventilation, and 1.52 (1.18-1.97) in areas with IEQ complaints. The effect of ventilation was independent of IEQ complaints and among those exposed to lower outdoor air supply rates the attributable risk of short-term sick leave was 35%. The cost of sick leave attributable to ventilation at current recommended rates was estimated as $480 per employee per year at Polaroid. These findings suggest that net savings of $400 per employee per year may be obtained with increased ventilation. Thus, currently recommended levels of outdoor air supply may be associated with significant morbidity, and lost productivity on a national scale could be as much as $22.8 billion per year. Additional studies of IEQ impacts on productivity and sick leave, and the mechanisms underlying the apparent association are needed.

Characterization and variability of endotoxin and 3-hydroxy fatty acids in an office building during a particle intervention study.

Air and dust samples were collected on two floors of an office building during a double-blind particle intervention study to examine spatial and temporal variability of airborne endotoxin over a period of weeks, and to characterize endotoxin activity and lipopolysaccharide (LPS) content in carpet and chair dust. Air samples were collected on multiple days within and across weeks. Dust samples were collected from carpets and chairs one day per week for three weeks. Endotoxin was measured using a Limulus assay. Dust samples were analyzed for LPS by determination of 3-hydroxy fatty acids (3-OHFAs) using gas chromatography-mass spectrometry. The geometric mean (geometric standard deviation) for 96 indoor air samples was 0.24 (1.6) EU/m3. Significant within-floor spatial variation of airborne endotoxin was found (P < 0.0001, n = 80). Temporal variability of airborne endotoxin was not significant across weeks. Mean (+/- SD) endotoxin levels in carpet dust (59 +/- 9.3 EU/mg dust, n = 12) and in chair dust (38 +/- 7.7 EU/mg dust, n = 10) were significantly different (P < 0.001). Carbon chain length-dependent differences in 3-OHFA levels by dust source and floor were found. Enhanced air filtration did not significantly affect airborne endotoxin (P = 0.62); however, total dust mass and total endotoxin in carpet dust samples increased significantly after enhanced surface cleaning (P < 0.01). These findings suggest that spatial variability, dust source, and surface cleaning may influence building occupant exposures to endotoxin.

Preliminary report on the results of the second phase of a round- robin endotoxin assay study using cotton dust.

In an on-going endotoxin assay study, a two-part interlaboratory endotoxin assay study has been completed. The purpose of the study was to compare the variation in assay results between different laboratories, and, if the variation was high, to see if a common protocol would reduce the variation. In both parts of the study, membrane filters laden with the same approximate amount and type of cotton dust were sent for analysis to laboratories that "routinely" perform endotoxin analyses. First, each of these laboratories performed the analysis using the methodology common to its laboratory. In the second part of the study, membrane filters with cotton dust were again sent to the same laboratories where the analyses were performed as before but with a common extraction protocol. The preliminary results from the first phase of the study have been collected and showed that intra-laboratory variations were small, but large and significant interlaboratory variation was observed. The results were reported elsewhere. The preliminary results from the second part of the study consisting of the data currently collected are presented here. Again, intra-laboratory variations were small, but, also again, large and significant inter-laboratory variation was observed. However, in this part of the study, the range between the highest and lowest average results was narrower than in the first part of the study. Influence of the assay kit type was examined. The variation within assay kit type was small but significant differences in results were observed between assay kit types. The findings suggest that endotoxin concentration in samples can be ranked within laboratories, but not necessarily between laboratories. However, some of the variation between laboratories has been reduced by a common extraction protocol which suggests the possibility of further standardization that may lead to better comparability between laboratories.

Predictors of repeated wheeze in the first year of life: the relative roles of cockroach, birth weight, acute lower respiratory illness, and maternal smoking.

While more than 80% of childhood asthmatics are allergic to one or more inhaled allergens, the role of inhaled allergens in the induction of wheeze in the first year of life is unknown. In a prospective birth-cohort study of 499 children of asthmatic/allergic parents from metropolitan Boston, we examined home allergen concentrations measured within the first 3 mo of life as predictors of repeated wheeze episodes in the first year of life. In multivariate analyses adjusting for maternal asthma and dog in the home, predictors of two or more wheeze episodes in the first year of life included maternal smoking during pregnancy (relative risk [RR] = 1.83; 95% confidence limit [CL]: 1.12, 3.00), lower respiratory illness in the first year of life (croup, bronchitis, bronchiolitis, or pneumonia) (RR = 2.25; 95% CL:1.58, 3.19), low birthweight (RR = 1.28, 95% confidence interval [CI]: 1.04, 1.58 for an interquartile difference), and Bla g 1 or 2 (cockroach) allergen level in the family room > 0.05 U/g dust (RR = 1.76; 95% CL: 1.20, 2.57). Cockroach allergen in the family room and repeated wheeze remained significant after adjustment for socioeconomic factors including race and income (RR = 1.63; 95% CL: 1.05, 2.55). It is unknown whether the association between cockroach and repeated wheeze in infancy represents a cockroach-related increased risk of bronchial inflammation through nonallergenic or allergenic mechanisms.

Occupational asthma and contact dermatitis in a spray painter after introduction of an aziridine cross-linker.

A 23-year-old spray painter developed contact dermatitis and respiratory difficulty characterized by small airways obstruction shortly after the polyfunctional aziridine cross-linker CX-100 began to be used in his workplace as a paint activator. The symptoms resolved after he was removed from the workplace and was treated with inhaled and topical steroids. Painters may have an increased risk of asthma due to exposure to a variety of agents, such as isocyanates, alkyd resins, and chromates. This case illustrates the importance of using appropriate work practices and personal protective equipment to minimize exposure. Occupational asthma is diagnosed by a history of work-related symptoms and exposure to known causative agents. The diagnosis is confirmed by serial pulmonary function testing or inhalational challenge testing. The risk of asthma attributable to occupational exposures is probably underappreciated due to underreporting and to inappropriate use of narrow definitions of exposure in epidemiologic studies of attributable risk.

The effects of carpet fresheners and other additives on the behaviour of indoor allergen assays.

BACKGROUND: Chemical agents such as tannic acid and detergents have been shown to introduce non-random bias in allergen measurement. OBJECTIVE: We investigated how several substances that are commonly found in floor dust (carpet fresheners, powdered pesticides, and table salt) affected immunoassays of purified standard allergens. METHODS: Three sets of experiments were conducted to: (1) screen for interference with allergen enzyme-linked immunosorbent assay (ELISA); (2) test for concentration-response; and (3) assess the site-of-action of a given dust additive (i.e. the effect on allergen binding to primary or secondary antibody). The ELISAs are commercially available two-site monoclonal antibody assays for Der p 1, Der f 1, and Fel d 1, and a monoclonal/polyclonal assay for Bla g 1. Outcomes are reported in terms of reaction rate (colour change per unit time), which is directly proportional to the amount of bound allergen. RESULTS: In the initial screening experiments, carpet fresheners tended to decrease Der p 1 assay reaction rates, increase Der f 1 assay rates, and produce little change in Fel d 1 assay rates. Three carpet fresheners decreased Der p 1 assay rate responses in a concentration-dependent manner. Two carpet fresheners noticeably increased Der f 1 assay reaction rates in both the screening and the concentration-response tests. Powdered pesticides increased reaction rates in the Bla g 1 assays and increased the slope of the dilution curve compared with that of the purified allergen. Salt decreased the reaction rates of Bla g 1 assays at allergen concentrations greater than 0.01 U/mL. For each of the four allergens, the largest effects of dust additives occurred when secondary antibody binding was altered. CONCLUSIONS: Some common household dust components can introduce systematic error into immunoassays for arthropod allergens.

Hierarchical cluster analysis applied to workers' exposures in fiberglass insulation manufacturing.

The objectives of this study were to explore the application of cluster analysis to the characterization of multiple exposures in industrial hygiene practice and to compare exposure groupings based on the result from cluster analysis with that based on non-measurement-based approaches commonly used in epidemiology. Cluster analysis was performed for 37 workers simultaneously exposed to three agents (endotoxin, phenolic compounds and formaldehyde) in fiberglass insulation manufacturing. Different clustering algorithms, including complete-linkage (or farthest-neighbor), single-linkage (or nearest-neighbor), group-average and model-based clustering approaches, were used to construct the tree structures from which clusters can be formed. Differences were observed between the exposure clusters constructed by these different clustering algorithms. When contrasting the exposure classification based on tree structures with that based on non-measurement-based information, the results indicate that the exposure clusters identified from the tree structures had little in common with the classification results from either the traditional exposure zone or the work group classification approach. In terms of the defining homogeneous exposure groups or from the standpoint of health risk, some toxicological normalization in the components of the exposure vector appears to be required in order to form meaningful exposure groupings from cluster analysis. Finally, it remains important to see if the lack of correspondence between exposure groups based on epidemiological classification and measurement data is a peculiarity of the data or a more general problem in multivariate exposure analysis.