Influence of housing characteristics on bacterial and fungal communities in homes of asthmatic children.

Variations in home characteristics, such as moisture and occupancy, affect indoor microbial ecology as well as human exposure to microorganisms. Our objective was to determine how indoor bacterial and fungal community structure and diversity are associated with the broader home environment and its occupants. Next-generation DNA sequencing was used to describe fungal and bacterial communities in house dust sampled from 198 homes of asthmatic children in southern New England. Housing characteristics included number of people/children, level of urbanization, single/multifamily home, reported mold, reported water leaks, air conditioning (AC) use, and presence of pets. Both fungal and bacterial community structures were non-random and demonstrated species segregation (C-score, P < 0.00001). Increased microbial richness was associated with the presence of pets, water leaks, longer AC use, suburban (vs. urban) homes, and dust composition measures (P < 0.05). The most significant differences in community composition were observed for AC use and occupancy (people, children, and pets) characteristics. Occupant density measures were associated with beneficial bacterial taxa, including Lactobacillus johnsonii as measured by qPCR. A more complete knowledge of indoor microbial communities is useful for linking housing characteristics to human health outcomes. Microbial assemblies in house dust result, in part, from the building's physical and occupant characteristics.

An environmental epigenetic study of ADRB2 5'-UTR methylation and childhood asthma severity.

BACKGROUND: Beta-2 adrenergic receptor (ADRB2) is the primary target of both short- and long-acting beta-agonist asthma medications. ADRB2 5'-UTR methylation changes in blood have the potential to act as a surrogate biomarker of responsiveness to beta-agonist treatment and childhood asthma severity. OBJECTIVE: To study the association between ADRB2 5'-UTR methylation, NO (2) exposure and childhood asthma severity. METHODS: We compared ADRB2 5'-UTR methylation levels in blood between 60 children with mild asthma and 122 children with severe asthma using methylation-specific PCR. We also investigated potential joint effects between NO (2) exposure and ADRB2 5'-UTR methylation. RESULTS: We found a significant association between intermediate (OR: 4.11, 95% CI: 1.58-10.73) and high levels (OR: 7.63, 95% CI: 3.02-19.26) of ADRB2 methylation and severe childhood asthma. In addition, we found a significant association between indoor exposure to NO (2) , an air pollutant and known asthmogen, and severe asthma among children exhibiting high ADRB2 methylation (OR: 4.59, 95% CI: 1.03-20.55) but no association among children exhibiting low levels of ADRB2 methylation (OR: 0.35, 95% CI: 0.01-14.13). CONCLUSIONS AND CLINICAL RELEVANCE: These findings support the potential use of ADRB2 5'-UTR methylation as a biomarker of both asthma severity and risk for NO (2) -associated asthma exacerbations in children, and present the first evidence of an epigenetic link between an important environmental exposure and childhood asthma severity.

Air pollutant emissions from kerosene space heaters.

Air pollutant emissions from portable convective and radiant kerosene space heaters were measured in an environmental chamber. Emission factors for nitrogen oxides, sulfur dioxide, carbon monoxide, carbon dioxide, and oxygen depletion are presented. The data suggest that the use of such heaters in residences can result in exposures to air pollutants in excess of ambient air quality standards and in some cases in excess of occupational health standards.

Use of hair colouring products and risk of multiple myeloma among US women.

OBJECTIVE: To evaluate the association between personal hair dye use and risk of multiple myeloma among women. METHODS: A population-based case-control study of 175 cases of multiple myeloma and 679 controls. Cases and controls were interviewed regarding the type and colour of hair colouring product used, age at first use, age use stopped, duration, and the frequency of use per year. Odds ratios (ORs) and 95% confidence intervals (CI) were estimated using unconditional logistic regression to compare never users with four exposure groups: all users, ever semi-permanent dye users, ever permanent dye users and dark permanent dye users (most frequent use). RESULTS: No association was found between ever reporting hair colouring product use and myeloma risk among all users (OR 0.8; 95% CI 0.5 to 1.1), semi-permanent dye users (OR 0.7; 95% CI 0.4 to 1.2), permanent dye users (OR 0.8; 95% CI 0.5 to 1.1) or dark permanent dye users (OR 0.8; 95% CI 0.5 to 1.3). There were no significant associations among women who used hair dyes before 30 years of age, started use before 1980, had >or=240 lifetime applications, or had used dark permanent dye for 28 or more years. CONCLUSION: No evidence of an association between hair colouring product use and myeloma risk was found. However, given the conflicting body of literature on hair colouring product use and risk of multiple myeloma, this question should be further evaluated in larger studies or consortia, and in high risk groups.

Traffic-related air pollution associations with cytokeratin-18, a marker of hepatocellular apoptosis, in an overweight and obese paediatric population.

INTRODUCTION: Traffic-related air pollution causes fatty liver, inflammation and fibrosis in animal models, but there have been few studies in humans. OBJECTIVES: To test the hypothesis that traffic-related air pollution causes non-alcoholic fatty liver disease (NAFLD) and increased markers for non-alcoholic steatohepatitis (NASH); and that NAFLD increases liver susceptibility to increased NASH risk. METHODS: Data collected prospectively from 74 overweight or obese children were obtained from the Yale Pediatric Obesity Clinic. Traffic-related air pollution was characterized as vehicle traffic volume on major roads within a 1 km residential buffer, and as residential nitrogen dioxide (NO2 ) exposure. Outcomes were hepatic fat fraction (HFF) measured by magnetic resonance imaging, liver enzymes using standard assays and plasma cytokeratin-18 (CK-18) by immunosorbent assays. RESULTS: Significant non-linear relationships with air pollution and CK-18 were found. Plasma CK-18 at follow-up increased from approximately 150 U/L to almost 200 U/L as residential traffic volume increased from 220 000 vehicle-km to 330 000 vehicle-km, after adjustment for baseline CK-18, age and gender. Among patients with NAFLD at baseline, CK-18 increased from 140 U/L to 200 U/L (a 1.5 standard deviation increase in CK-18) as NO2 increased from 8 to 10 ppb. CONCLUSIONS: Traffic-related air pollution was associated with CK-18. Effects were larger in children with pre-existing NAFLD at study entry.

Comparison of parental reports of smoking and residential air nicotine concentrations in children.

BACKGROUND: Using questionnaires to assess children's residential exposure to environmental tobacco smoke (ETS) may result in misclassification from recall and response bias. Questionnaire data have frequently been validated against urinary cotinine measurements, but rarely against actual measurements of residential air nicotine. OBJECTIVE: To compare questionnaire reported smoking with air nicotine concentrations in a large population of children and with urinary cotinine levels in a subpopulation; and to assess the potential impact of the symptom status of the children on the agreement between different measures of exposure. METHODS: The authors assessed residential exposure to ETS in 347 German, 335 Dutch, and 354 Swedish preschool and schoolchildren by questionnaire and air nicotine measurements, and in a subset of 307 German children by urinary cotinine measurements. They then compared the different measures of ETS exposure. RESULTS: In all countries, air nicotine concentrations increased with increasing questionnaire reported smoking in a dose-response fashion. Specificity and negative predictive values of questionnaire reports for nicotine concentrations were excellent. Sensitivity and positive predictive values were moderate to good. Excluding occasional smokers, the overall percentage of homes misclassified was 6.9%, 6.7%, and 5.1% in Germany, the Netherlands, and Sweden, respectively. Similar results were found for the agreement of urinary cotinine concentrations with questionnaire reports and air nicotine levels. There was no indication of underreporting by parents of symptomatic children. CONCLUSION: Despite some misclassification, questionnaire reports are an inexpensive and valid estimate of residential ETS exposure among preschool and school children.

Indoor exposures to fine aerosols and acid gases.

Indoor exposures to aerosols and gases are associated with both indoor and outdoor air pollution sources. The identification of sources and the assessment of their relative contribution can be a complicated process due to a) the presence of numerous indoor sources, which can vary from building to building; b) the uncertainties associated with the estimation of the impact of outdoor sources on indoor air quality; c) the interactions between pollutants; and d) the importance of reactions between pollutants and indoor surfaces. It is well established that fine particles (diameter less than or equal to 2.5 microns) originating from outdoor sources such as automobiles, oil and coal combustion, incineration, and diverse industrial activities can penetrate into the indoor environment. Indoor/outdoor ratios, usually varying between 0.4 and 0.8, depend on parameters such as particle size and density, air exchange rate, and the surface-to-volume ratio of the indoor environment. Determining fine particle elemental composition makes it possible to identify the contribution of different outdoor sources. This paper focuses on the origin and the concentration of indoor aerosols and acid gases by highlighting the results from two indoor air quality studies.

Assessing exposures to inhaled complex mixtures.

In the course of daily activities, individuals spend varying amounts of time in different spaces where they are exposed to a complex mixture of gas, vapor, and particulate contaminants. The term complex is used in this paper to refer to binary mixtures as well as truly complex mixtures of three or more constituents. The diversity of the environments where pollution may occur, the number of pollutants that may be present, and the nature of the activity in the environment combine to pose a challenge to investigators of the health effects of air pollutants. This article discusses several methods of measuring or assessing exposure to complex mixture air contaminants that include time-activity assessments, personal monitoring, biomarkers of exposure, and microenvironmental models that can be employed singly or in combination in a protocol for exposure assessment. The use of nested designs, involving more intensive data collection from samples or subjects, is also considered.

Effect of nitrous acid on lung function in asthmatics: a chamber study.

Nitrous acid, a component of photochemical smog and a common indoor air pollutant, may reach levels of 100 ppb where gas stoves and unvented portable kerosene heaters are used. Nitrous acid is a primary product of combustion and may also be a secondary product by reaction of nitrogen dioxide with water. Because the usual assays for nitrogen dioxide measure several oxides of nitrogen (including nitrous acid) together, previous studies of indoor nitrogen dioxide may have included exposure to and health effects of nitrous acid. To assess the respiratory effects of nitrous acid exposure alone, we carried out a double-blinded crossover chamber exposure study with 11 mildly asthmatic adult subjects. Each underwent 3-hr exposures to 650 ppb nitrous acid and to filtered room air with three 20-min periods of moderate cycle exercise. Symptoms, respiratory parameters during exercise, and spirometry after exercise were measured. A statistically significant decrease in forced vital capacity was seen on days when subjects were exposed to nitrous acid. This effect was most marked at 25 min and 85 min after exposure began. Aggregate respiratory and mucous membrane symptoms were also significantly higher with nitrous acid. We conclude that this concentration and duration of exposure to nitrous acid alters lung mechanics slightly, does not induce significant airflow obstruction, and produces mild irritant symptoms in asthmatics.

Indoor, outdoor, and regional summer and winter concentrations of PM10, PM2.5, SO4(2)-, H+, NH4+, NO3-, NH3, and nitrous acid in homes with and without kerosene space heaters.

Twenty-four-hour samples of PM10 (mass of particles with aerodynamic diameter < or = 10 microm), PM2.5, (mass of particles with aerodynamic diameter < or = 2.5 microm), particle strong acidity (H+), sulfate (SO42-), nitrate (NO3-), ammonia (NH3), nitrous acid (HONO), and sulfur dioxide were collected inside and outside of 281 homes during winter and summer periods. Measurements were also conducted during summer periods at a regional site. A total of 58 homes of nonsmokers were sampled during the summer periods and 223 homes were sampled during the winter periods. Seventy-four of the homes sampled during the winter reported the use of a kerosene heater. All homes sampled in the summer were located in southwest Virginia. All but 20 homes sampled in the winter were also located in southwest Virginia; the remainder of the homes were located in Connecticut. For homes without tobacco combustion, the regional air monitoring site (Vinton, VA) appeared to provide a reasonable estimate of concentrations of PM2.5 and SO42- during summer months outside and inside homes within the region, even when a substantial number of the homes used air conditioning. Average indoor/outdoor ratios for PM2.5 and SO42- during the summer period were 1.03 +/- 0.71 and 0.74 +/- 0.53, respectively. The indoor/outdoor mean ratio for sulfate suggests that on average approximately 75% of the fine aerosol indoors during the summer is associated with outdoor sources. Kerosene heater use during the winter months, in the absence of tobacco combustion, results in substantial increases in indoor concentrations of PM2.5, SO42-, and possibly H+, as compared to homes without kerosene heaters. During their use, we estimated that kerosene heaters added, on average, approximately 40 microg/m3 of PM2.5 and 15 microg/m3 of SO42- to background residential levels of 18 and 2 microg/m3, respectively. Results from using sulfuric acid-doped Teflon (E.I. Du Pont de Nemours & Co., Wilmington, DE) filters in homes with kerosene heaters suggest that acid particle concentrations may be substantially higher than those measured because of acid neutralization by ammonia. During the summer and winter periods indoor concentrations of ammonia are an order of magnitude higher indoors than outdoors and appear to result in lower indoor acid particle concentrations. Nitrous acid levels are higher indoors than outdoors during both winter and summer and are substantially higher in homes with unvented combustion sources.

The accuracy of environmental tobacco smoke exposure measures among asthmatic children.

This study determined the reliability and validity of parent-reported measures of environmental tobacco smoke (ETS) exposure among 91 asthmatic children. Test-retest reliability assessments were conducted for environmental, biological and parent-reported measures of ETS exposure. All measures except a urine cotinine assay resulted in satisfactory levels of reliability. The parent-reported measures of ETS exposure were compared to the environmental filter measure of nicotine as well as submitted to a construct validity test. Parent-reported home exposure to ETS proved moderately and significantly correlated to the filter measure. Approximately 80% of all hypothetical constructs agreed with the observed relationships for convergent, divergent and discriminant validity. It was concluded that middle class Caucasian parents' reports of their asthmatic child's residential ETS exposure are reliable and valid. These parent-reported measures should be valuable tools for epidemiological investigations and for clinical programs designed to reduce asthmatic children's residential exposure to ETS.

Reduction of environmental tobacco smoke exposure among asthmatic children: a controlled trial.

STUDY OBJECTIVE: This randomized clinical trial tested a behavioral medicine program designed to reduce asthmatic children's exposure to environmental tobacco smoke (ETS) in the home. DESIGN: Families were randomly assigned to an experimental preventive medicine counseling group, a monitoring control group, or a usual treatment control group. Families were measured six times over 1 year. PARTICIPANTS: Ninety-one families were recruited from four allergy clinics. INTERVENTION: The experimental group received a 6-month series of counseling sessions designed to decrease ETS exposure. This group also monitored smoking, exposure, and children's asthma symptoms. The monitoring group did not receive counseling and the usual treatment control group received outcome measures only. MEASUREMENTS AND RESULTS: Parents reported the daily number of cigarettes children were exposed to during the week preceding interviews. A nicotine air monitor and construct validity analysis confirmed the validity of exposure reports. Exposure to the parent's cigarettes in the home decreased for all groups. The experimental group attained a 79 percent decrease in children's ETS exposure, compared with 42 percent for the monitoring control and 34 percent for the usual treatment control group. Repeated-measures analysis of variance resulted in a significant (F([10,350] = 1.92, p < 0.05) group by time effect. At the final 12-month visit, the experimental/counseling group sustained a 51% decrease in children's exposure to cigarettes in the home from all smokers, while the monitoring control group showed an 18% decrease and the usual treatment control group a 15% decrease from pre-intervention [corrected]. CONCLUSION: A behavioral medicine program was successful in reducing exposure to ETS in the home for these asthmatic children.

Comparisons of seasonal fungal prevalence in indoor and outdoor air and in house dusts of dwellings in one Northeast American county.

Fungi cause allergies and many other adverse health effects. In this study, we characterized the nature and seasonal variation of fungi inside and outside homes in the Greater New Haven, Connecticut area. Three indoor air samples (in the living room, bedroom, and basement) and one outdoor sample were collected by the Burkard portable air sampler. House dust samples were collected in the living room by a vacuum cleaner. The mold concentrations varied widely from house to house in both indoor and outdoor air. No significant difference (p>0.05) in concentration and type of fungi between living room and bedroom or by season was observed. Both concentration and type of fungi were significantly higher (p<0.05) in the basement than other indoor areas and outdoor air in winter. The type of fungi in living room, bedroom, and outdoor air were found to have significant changes among seasons, but there was no significant difference for the basement among seasons. Cladosporium spp. was dominant in both indoor and outdoor air in summer. Penicillium and Aspergillus were dominant in indoor air in winter, but neither was dominant in any season in outdoor air. The type of fungi and their concentrations in house dust samples were not representative of those isolated in indoor air. In dust samples, more Mucor, Wallemia, and Alternaria species, but less Aspergillus, Cladosporium, and Penicillium species were found in all seasons. Air sampling in spring or fall in every suspected house is suggested for year-round fungal exposure assessment.

Indoor and outdoor PM2.5 and CO in high- and low-density Guatemalan villages.

Continuous particles less than 2.5 microm in diameter (PM2.5) and carbon monoxide (CO) were monitored during breakfast, lunch, and dinner in three high-density and four low-density villages near Quetzaltenango, Guatemala to help assess the viability of this region for a proposed respiratory health and stove intervention study. Approximately 15 homes were visited during each mealtime in each of the seven villages; in all, 98 homes were visited, with a sampling duration of 2-3 min per home per meal. For each village, a line (transect) was drawn on a village map along existing roads from one end of the village to the other; homes and between-home outside locations along the transect were monitored. Although the predominant stove type was the open fire, several other stoves, in various levels of disrepair, were observed frequently. The highest indoor concentrations of PM2.5 were observed in homes using the open fire (avg. = 5.31 mg/m3; SD=4.75 mg/m3) or equivalent, although homes using the plancha--indigenous wood-burning stove with chimney--also had measurements > 13.8 mg/m3, PM2.5 limit of detection. The highest indoor concentrations of CO were also observed in homes using the open fire (avg. = 22.9 ppm; SD = 28.1 ppm), with a maximum measurement of > 250 ppm. For both PM2.5 and CO, levels measured in homes with plancha, lorena, or open fire were significantly higher than levels taken in the street or in homes using a gas stove. The Spearman correlation coefficient between PM2.5 and CO for all data combined was 0.81, and ranged from 0.30 for the lorena to 0.68 for the plancha in homes using wood-fueled stoves. Although indoor PM2.5 and CO levels were not significantly different between high- and low-density villages, street-level PM2.5 (p = 0.002) and CO (p= 0.002), were significantly higher in the high - density villages. These data provide a useful picture of the pollution levels coming from a range of cooking stoves in various levels ofdisrepair, as well as a representation of how outdoor particle mass and CO levels vary from high- versus low-density villages.

An evaluation of respiratory effects following exposure to 2.0 ppm formaldehyde in asthmatics: lung function, symptoms, and airway reactivity.

Fifteen asthmatic volunteers were exposed in a double-blind, random manner to room air and 2.0 ppm formaldehyde for 40 min in an environmental chamber. These exposures were repeated on a separate day during moderate exercise (450 kpm/min) for 10 min. Ambient and dew point temperatures were 23.0 +/- 0.0 degrees C and 11.5 +/- 1.0 degrees C, respectively. No significant airway obstruction as measured by flow-volume parameters and airway resistance was noted in this group during or immediately after exposure. Furthermore, sequential measurements of peak flow for 24 hr following formaldehyde exposure revealed no delayed airway response. In contrast, in comparison to the baseline methacholine inhalation challenge (MIC) test on the screening day, 8 of 12 asthmatics demonstrated a lower threshold to MIC following 2.0 ppm exposure for 40 min; however, the mean and median decrements of threshold in methacholine concentration of 10.4 mg/ml and 24.3 mg/ml were not significant (p = .12). Bad odor, sore throat, and eye irritation were common during exposure but symptoms were infrequent afterward.

A study of respiratory effects from exposure to 2 ppm formaldehyde in healthy subjects.

Formaldehyde (FA) is a common indoor air pollutant with irritative properties. It has been suggested that FA may produce physiologic alterations of the respiratory system. To study such responses, 15 nonsmoking, healthy subjects were exposed in a double blind, random manner to 0 and 2 ppm FA for 40 min in an environmental chamber. In addition, the same exposures were repeated on a separate day with the subjects performing moderate exercise (450 kpm/min) for 10 min. Exposures were carried out under controlled environmental conditions (temperature = 23 degrees C, relative humidity = 50%). Pulmonary function was measured before, during, and after exposures using partial and maximal flow-volume curves and airway resistance. Symptom diaries were given to the subjects; upper and lower airway symptoms were recorded for up to 24 hr following exposures. No significant bronchoconstriction was noted in this group. In 3 subjects, sequential measurements of peak flow over a 24-hr period following FA exposure failed to reveal any delayed airway response. On a separate day, 6 healthy subjects failed to demonstrate changes from their baseline responsiveness to methacholine after exposure to 2 ppm FA. Respiratory symptoms were, in general, confined to the upper airways and were mild to moderate in severity. We conclude that short exposures to 2 ppm FA do not result in acute or subacute changes in lung function among healthy individuals either at rest or with exercise. Subjective complaints following such exposures are confined to irritative phenomena of the upper airways.

Airway effects of low concentrations of sulfur dioxide: dose-response characteristics.

The acute respiratory effects of exposure to low-level, short-term sulfur dioxide (SO2) were studied in ten asthmatic and ten healthy subjects. Subjects were exposed in an environmental chamber in a double-blind, random sequence to SO2) levels of 0.00, 0.25, 0.50, 0.75, and 1.00 ppm for 40 min. During the first 10 min subjects exercised on a cycloergometer at a level of 450 kpm/min. On separate days, subjects were exposed to 0 and 1.0 ppm SO2 in the absence of exercise. In exercising asthmatic subjects, breathing 1 ppm SO2 resulted in significant changes from baseline in airway resistance (Raw), forced expiratory volume in 1 sec (FEV1.0), maximal expiratory flow at 60% of the vital capacity (VC) below total lung capacity on the partial flow volume curve [MEF40% (P)] as well as reductions in flows at 50% of VC (Vmax50%). None of these parameters showed significant changes for exposures to 0.5 ppm or less, with the exception of small decreases (i.e., less than 0.2 L/sec) in Vmax50% at 0.25 and 0.5 ppm. Ten minutes after the end of exercise, there were no statistically significant differences from baseline, even though SO2 was still present in the chamber atmosphere. For asthmatic subjects, the average changes in Raw, FEV1.0, MEF40%(P), and Vmax50% increased as SO2 levels increased, suggestive of a dose-response relationship with a consistent effect first seen at 0.75 ppm. In individual exercising asthmatics, responses may occur at levels of SO2 below 0.75 ppm. No changes were seen in healthy individuals on any day, or in asthmatic subjects at rest.(ABSTRACT TRUNCATED AT 250 WORDS)

Stability of tobacco smoke odor in enclosed spaces.

During each of five experiments, four sedentary subjects smoked a total of 8 cigarettes during one hour while occupying an odor test chamber. The air temperature was 20-22 degrees C and the relative humidity was 35-50%. During the entire test period (6 h) the odor intensity in the chamber was evaluated by judges. After smoking ceased, the odor intensity continued to rise for one or two hours and then remained constant in a way that is characteristic of unreactive contaminants.

Indoor nitrous acid and respiratory symptoms and lung function in adults.

BACKGROUND: Nitrogen dioxide (NO2) is an important pollutant of indoor and outdoor air, but epidemiological studies show inconsistent health effects. These inconsistencies may be due to failure to account for the health effects of nitrous acid (HONO) which is generated directly from gas combustion and indirectly from NO2. METHODS: Two hundred and seventy six adults provided information on respiratory symptoms and lung function and had home levels of NO2 and HONO measured as well as outdoor levels of NO2. The association of indoor HONO levels with symptoms and lung function was examined. RESULTS: The median indoor HONO level was 3.10 ppb (IQR 2.05-5.09), with higher levels in homes with gas hobs, gas ovens, and in those measured during the winter months. Non-significant increases in respiratory symptoms were observed in those living in homes with higher HONO levels. An increase of 1 ppb in indoor HONO was associated with a decrease in forced expiratory volume in 1 second (FEV1) percentage predicted (-0.96%; 95% CI -0.09 to -1.82) and a decrease in percentage FEV1/forced vital capacity (FVC) (-0.45%; 95% CI -0.06 to -0.83) after adjustment for relevant confounders. Measures of indoor NO2 were correlated with HONO (r = 0.77), but no significant association of indoor NO2 with symptoms or lung function was observed. After adjustment for NO2 measures, the association of HONO with low lung function persisted. CONCLUSION: Indoor HONO levels are associated with decrements in lung function and possibly with more respiratory symptoms. Inconsistencies between studies examining health effects of NO2 and use of gas appliances may be related to failure to account for this association.