Cow allergen (Bos d2) and endotoxin concentrations are higher in the settled dust of homes proximate to industrial-scale dairy operations.

Airborne contaminants produced by industrial agricultural facilities contain chemical and biological compounds that can impact the health of residents living in close proximity. Settled dust can be a reservoir for these contaminants and can influence long-term exposures. In this study, we sampled the indoor- and outdoor-settled dust from 40 homes that varied in proximity to industrial-scale dairies (ISD; industrial-scale dairy, a term used in this paper to describe a large dairy farm and adjacent waste sprayfields, concentrated animal feeding operation or animal feeding operation, that uses industrial processes) in the Yakima Valley, Washington. We analyzed settled dust samples for cow allergen (Bos d2, a cow allergen associated with dander, hair, sweat and urine, it is a member of the lipocalin family of allergens associated with mammals), mouse allergen (Mus m1; major mouse allergen, a mouse urinary allergen, in the lipocalin family), dust mite allergens (Der p1 (Dermatophagoides pteronissinus 1) and Der f1 (Dermatophagoides farinae 1)), and endotoxin (a component of the cell walls of gram negative bacteria, lipopolysaccharide, which can be found in air and dust and can produce a strong inflammatory response). A concentration gradient was observed for Bos d2 and endotoxin measured in outdoor-settled dust samples based on proximity to ISD. Indoor-settled dust concentrations of Bos d2 and endotoxin were also highest in proximal homes. While the associated health effects of exposure to cow allergen in settled dust is unknown, endotoxin at concentrations observed in these proximal homes (100 EU/mg) has been associated with increased negative respiratory health effects. These findings document that biological contaminants emitted from ISDs are elevated in indoor- and outdoor-settled dust samples at homes close to these facilities and extend to as much as three miles (4.8 km) away.

Characterization of a portable method for the collection of exhaled breath condensate and subsequent analysis of metal content.

Using exhaled breath condensate (EBC) as a biological media for analysis of biomarkers of exposure may facilitate the understanding of inhalation exposures. In this study, we present method validation for the collection of EBC and analysis of metals in EBC. The collection method was designed for use in a small scale longitudinal study with the goal of improving reproducibility while maintaining economic feasibility. We incorporated the use of an Rtube with additional components as an assembly, and trained subjects to breathe into the apparatus. EBC was collected from 8 healthy adult subjects with no known elevated exposures to Mn, Cr, Ni, and Cd repeatedly (10 times) within 7 days and analyzed for these metals via ICP-MS. Method detection limits were obtained by mimicking the process of EBC collection with ultrapure water, and resulted in 46-62% of samples falling in a range less than the method detection limit. EBC metal concentrations were found to be statistically significantly associated (p < 0.05) with room temperature and relative humidity during collection, as well as with the gender of the subject. The geometric mean EBC metal concentrations in our unexposed subjects were 0.57 µg Mn per L, 0.25 µg Cr per L, 0.87 µg Ni per L, and 0.14 µg Cd per L. The overall standard deviation was greater than the mean estimate, and the major source in EBC metals concentrations was due to fluctuations in subjects' measurements over time rather than to the differences between separate subjects. These results suggest that measurement and control of EBC collection and analytical parameters are critical to the interpretation of EBC metals measurements. In particular, rigorous estimation of method detection limits of metals in EBC provides a more thorough evaluation of accuracy.

Assessment of heterogeneity of metal composition of fine particulate matter collected from eight U.S. counties using principal component analysis.

The main objectives of this study are to (1) characterize chemical constituents of particulate matter (PM) and (2) compare overall differences in PM collected from eight US. counties. This project was undertaken as a part of a larger research program conducted by the Johns Hopkins Particulate Matter Research Center (JHPMRC). The goal of the JHPMRC is to explore the relationship between health effects and exposure to ambient PM of differing composition. The JHPMRC collected weekly filter-based ambient fine particle samples from eight US. counties between January 2008 and January 2010. Each sampling effort consisted of a 5-6-week sampling period. Filters were analyzed for 25 metals using inductively coupled plasma mass spectrometry (ICP-MS). Overall compositional differences were ranked by principal component analysis (PCA). The results showed that weekly concentrations of each element varied 3-40 times between the eight counties. PCA showed that the first five principal components explained 85% of the total variance. The authors found significant overall compositional differences in PM as the average of standardized principal component scores differed between the counties. These findings demonstrate PCA is a useful tool to identify the differences in PM compositional mixtures by county. These differences will be helpful for epidemiological and toxicological studies to help explain why health risks associated with PM exposure are different in locations with similar mass concentrations of PM.

Particulate matter air pollution disrupts endothelial cell barrier via calpain-mediated tight junction protein degradation.

BACKGROUND: Exposure to particulate matter (PM) is a significant risk factor for increased cardiopulmonary morbidity and mortality. The mechanism of PM-mediated pathophysiology remains unknown. However, PM is proinflammatory to the endothelium and increases vascular permeability in vitro and in vivo via ROS generation. OBJECTIVES: We explored the role of tight junction proteins as targets for PM-induced loss of lung endothelial cell (EC) barrier integrity and enhanced cardiopulmonary dysfunction. METHODS: Changes in human lung EC monolayer permeability were assessed by Transendothelial Electrical Resistance (TER) in response to PM challenge (collected from Ft. McHenry Tunnel, Baltimore, MD, particle size >0.1 µm). Biochemical assessment of ROS generation and Ca2+ mobilization were also measured. RESULTS: PM exposure induced tight junction protein Zona occludens-1 (ZO-1) relocation from the cell periphery, which was accompanied by significant reductions in ZO-1 protein levels but not in adherens junction proteins (VE-cadherin and ß-catenin). N-acetyl-cysteine (NAC, 5 mM) reduced PM-induced ROS generation in ECs, which further prevented TER decreases and atteneuated ZO-1 degradation. PM also mediated intracellular calcium mobilization via the transient receptor potential cation channel M2 (TRPM2), in a ROS-dependent manner with subsequent activation of the Ca2+-dependent protease calpain. PM-activated calpain is responsible for ZO-1 degradation and EC barrier disruption. Overexpression of ZO-1 attenuated PM-induced endothelial barrier disruption and vascular hyperpermeability in vivo and in vitro. CONCLUSIONS: These results demonstrate that PM induces marked increases in vascular permeability via ROS-mediated calcium leakage via activated TRPM2, and via ZO-1 degradation by activated calpain. These findings support a novel mechanism for PM-induced lung damage and adverse cardiovascular outcomes.

Use of X-ray absorption spectroscopy to speciate manganese in airborne particulate matter from five counties across the United States.

The purpose of this study is to characterize manganese oxidation states and speciation in airborne particulate matter (PM) and describe how these potentially important determinants of PM toxicity vary by location. Ambient PM samples were collected from five counties across the US using a high volume sequential cyclone system that collects PM in dry bulk form segregated into "coarse" and "fine" size fractions. The fine fraction was analyzed for this study. Analyses included total Mn using ICP-MS and characterization of oxidation states and speciation using X-ray absorption spectroscopy (XAS). XAS spectra of all samples and ten standard compounds of Mn were obtained at the National Synchrotron Light Source. XAS data was analyzed using Linear Combination Fitting (LCF). Results of the LCF analysis describe differences in composition between samples. Mn(II) acetate and Mn(II) oxide are present in all samples, while Mn(II) carbonate and Mn(IV) oxide are absent. To the best of our knowledge, this is the first paper to characterize Mn composition of ambient PM and examine differences between urban sites in the US. Differences in oxidation state and composition indicate regional variations in sources and atmospheric chemistry that may help explain differences in health effects identified in epidemiological studies.

Particulate matter induces cardiac arrhythmias via dysregulation of carotid body sensitivity and cardiac sodium channels.

The mechanistic links between exposure to airborne particulate matter (PM) pollution and the associated increases in cardiovascular morbidity and mortality, particularly in people with congestive heart failure (CHF), have not been identified. To advance understanding of this issue, genetically engineered mice (CREB(A133)) exhibiting severe dilated cardiomyopathic changes were exposed to ambient PM collected in Baltimore. CREB(A133) mice, which display aberrant cardiac physiology and anatomy reminiscent of human CHF, displayed evidence of basal autonomic aberrancies (compared with wild-type mice) with PM exposure via aspiration, producing significantly reduced heart rate variability, respiratory dysynchrony, and increased ventricular arrhythmias. Carotid body afferent nerve responses to hypoxia and hyperoxia-induced respiratory depression were pronounced in PM-challenged CREB(A133) mice, and denervation of the carotid bodies significantly reduced PM-mediated cardiac arrhythmias. Genome-wide expression analyses of CREB(A133) left ventricular tissues demonstrated prominent Na(+) and K(+) channel pathway gene dysregulation. Subsequent PM challenge increased tyrosine phosphorylation and nitration of the voltage-gated type V cardiac muscle α-subunit of the Na(+) channel encoded by SCN5A. Ranolazine, a Na(+) channel modulator that reduces late cardiac Na(+) channel currents, attenuated PM-mediated cardiac arrhythmias and shortened PM-elongated QT intervals in vivo. These observations provide mechanistic insights into the epidemiologic findings in susceptibility of human CHF populations to PM exposure. Our results suggest a multiorgan pathobiology inherent to the CHF phenotype that is exaggerated by PM exposure via heightened carotid body sensitivity and cardiac Na(+) channel dysfunction.

Airborne cow allergen, ammonia and particulate matter at homes vary with distance to industrial scale dairy operations: an exposure assessment.

BACKGROUND: Community exposures to environmental contaminants from industrial scale dairy operations are poorly understood. The purpose of this study was to evaluate the impact of dairy operations on nearby communities by assessing airborne contaminants (particulate matter, ammonia, and cow allergen, Bos d 2) associated with dairy operations inside and outside homes. METHODS: The study was conducted in 40 homes in the Yakima Valley, Washington State where over 61 dairies operate. RESULTS: A concentration gradient was observed showing that airborne contaminants are significantly greater at homes within one-quarter mile (0.4 km) of dairy facilities, outdoor Bos d 2, ammonia, and TD were 60, eight, and two times higher as compared to homes greater than three miles (4.8 km) away. In addition median indoor airborne Bos d 2 and ammonia concentrations were approximately 10 and two times higher in homes within one-quarter mile (0.4 km) compared to homes greater than three miles (4.8 km) away. CONCLUSIONS: These findings demonstrate that dairy operations increase community exposures to agents with known human health effects. This study also provides evidence that airborne biological contaminants (i.e. cow allergen) associated with airborne particulate matter are statistically elevated at distances up to three miles (4.8 km) from dairy operations.

A Scanning Transmission Electron Microscopy Method for Determining Manganese Composition in Welding Fume as a Function of Primary Particle Size.

Increasing evidence suggests that the physicochemical properties of inhaled nanoparticles influence the resulting toxicokinetics and toxicodynamics. This report presents a method using scanning transmission electron microscopy (STEM) to measure the Mn content throughout the primary particle size distribution of welding fume particle samples collected on filters for application in exposure and health research. Dark field images were collected to assess the primary particle size distribution and energy-dispersive X-ray and electron energy loss spectroscopy were performed for measurement of Mn composition as a function of primary particle size. A manual method incorporating imaging software was used to measure the primary particle diameter and to select an integration region for compositional analysis within primary particles throughout the size range. To explore the variation in the developed metric, the method was applied to 10 gas metal arc welding (GMAW) fume particle samples of mild steel that were collected under a variety of conditions. The range of Mn composition by particle size was -0.10 to 0.19 %/nm, where a positive estimate indicates greater relative abundance of Mn increasing with primary particle size and a negative estimate conversely indicates decreasing Mn content with size. However, the estimate was only statistically significant (p<0.05) in half of the samples (n=5), which all had a positive estimate. In the remaining samples, no significant trend was measured. Our findings indicate that the method is reproducible and that differences in the abundance of Mn by primary particle size among welding fume samples can be detected.

Design and characterization of a sequential cyclone system for the collection of bulk particulate matter.

In this paper, we describe the design, development and characterization of a high-volume sequential cyclone system for the collection of size-segregated PM in dry bulk form from the ambient environment in sufficient quantity for physical, chemical and toxicological characterization. The first stage of the system consists of a commercially available high volume PM(10) inlet. The second stage cyclone was designed by us to collect inhalable coarse particles (<10 µm and >2.5 µm). When tested individually with a challenge aerosol, a D(50) cut-size of this stage was found to be 2.3 µm at a flow rate of 1 m(3) min(-1). The third stage, a commercially available cyclone designed for surface dust sampling, had a D(50) cut-size of 0.3 µm when tested at the same flow rate. The purpose of the third stage is to collect the fine particle portion of PM(2.5) or accumulation mode (PM <2.5 µm and >0.1 µm). Thus, the sequential cyclone system will collect bulk samples of both the inhalable coarse particles and the fine particle portion of PM(2.5). The operation and maintenance of the new system are straightforward and allow for reliable collection of dry bulk ambient PM at relatively low cost.

Particulate matter disrupts human lung endothelial barrier integrity via ROS- and p38 MAPK-dependent pathways.

Epidemiologic studies have linked exposure to airborne pollutant particulate matter (PM) with increased cardiopulmonary mortality and morbidity. The mechanisms of PM-mediated lung pathophysiology, however, remain unknown. We tested the hypothesis that PM, via enhanced oxidative stress, disrupts lung endothelial cell (EC) barrier integrity, thereby enhancing organ dysfunction. Using PM collected from Ft. McHenry Tunnel (Baltimore, MD), we assessed PM-mediated changes in transendothelial electrical resistance (TER) (a highly sensitive measure of barrier function), reactive oxygen species (ROS) generation, and p38 mitogen-activated protein kinase (MAPK) activation in human pulmonary artery EC. PM induced significant dose (10-100 microg/ml)- and time (0-10 h)-dependent EC barrier disruption reflected by reduced TER values. Exposure of human lung EC to PM resulted in significant ROS generation, which was directly involved in PM-mediated EC barrier dysfunction, as N-acetyl-cysteine (NAC, 5 mM) pretreatment abolished both ROS production and barrier disruption induced by PM. Furthermore, PM induced p38 MAPK activation and HSP27 phosphorylation, events that were both attenuated by NAC. In addition, PM-induced EC barrier disruption was partially prevented by the p38 MAP kinase inhibitor SB203580 (10 microM) as well as by reduced expression of either p38 MAPK beta or HSP27 (siRNA). These results demonstrate that PM induces ROS generation in human lung endothelium, resulting in oxidative stress-mediated EC barrier disruption via p38 MAPK- and HSP27-dependent pathways. These findings support a novel mechanism for PM-induced lung dysfunction and adverse cardiopulmonary outcomes.

Emergency admissions for cardiovascular and respiratory diseases and the chemical composition of fine particle air pollution.

BACKGROUND: Population-based studies have estimated health risks of short-term exposure to fine particles using mass of PM(2.5) (particulate matter or= 65 years of age). RESULTS: In multiple-pollutant models that adjust for the levels of other pollutants, an interquartile range (IQR) increase in EC was associated with a 0.80% [95% posterior interval (PI), 0.34-1.27%] increase in risk of same-day cardiovascular admissions, and an IQR increase in OCM was associated with a 1.01% (95% PI, 0.04-1.98%) increase in risk of respiratory admissions on the same day. Other components were not associated with cardiovascular or respiratory hospital admissions in multiple-pollutant models. CONCLUSIONS: Ambient levels of EC and OCM, which are generated primarily from vehicle emissions, diesel, and wood burning, were associated with the largest risks of emergency hospitalization across the major chemical constituents of PM(2.5).

Regulation of COX-2 expression and IL-6 release by particulate matter in airway epithelial cells.

Particulate matter (PM) in ambient air is a risk factor for human respiratory and cardiovascular diseases. The delivery of PM to airway epithelial cells has been linked to release of proinflammatory cytokines; however, the mechanisms of PM-induced inflammatory responses are not well-characterized. This study demonstrates that PM induces cyclooxygenase (COX)-2 expression and IL-6 release through both a reactive oxygen species (ROS)-dependent NF-kappaB pathway and an ROS-independent C/EBPbeta pathway in human bronchial epithelial cells (HBEpCs) in culture. Treatment of HBEpCs with Baltimore PM induced ROS production, COX-2 expression, and IL-6 release. Pretreatment with N-acetylcysteine (NAC) or EUK-134, in a dose-dependent manner, attenuated PM-induced ROS production, COX-2 expression, and IL-6 release. The PM-induced ROS was significantly of mitochondrial origin, as evidenced by increased oxidation of the mitochondrially targeted hydroethidine to hydroxyethidium by reaction with superoxide. Exposure of HBEpCs to PM stimulated phosphorylation of NF-kappaB and C/EBPbeta, while the NF-kappaB inhibitor, Bay11-7082, or C/EBPbeta siRNA attenuated PM-induced COX-2 expression and IL-6 release. Furthermore, NAC or EUK-134 attenuated PM-induced activation of NF-kappaB; however, NAC or EUK-134 had no effect on phosphorylation of C/EBPbeta. In addition, inhibition of COX-2 partly attenuated PM-induced Prostaglandin E2 and IL-6 release.

Murine lung responses to ambient particulate matter: genomic analysis and influence on airway hyperresponsiveness.

BACKGROUND: Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Epidemiologic studies have demonstrated that exposures to environmental factors such as ambient particulate matter (PM), a major air pollutant, contribute to increased asthma prevalence and exacerbations. OBJECTIVE: We investigated pathophysiologic responses to Baltimore, Maryland, ambient PM (median diameter, 1.78 mum) in a murine model of asthma and attempted to identify PM-specific genomic/molecular signatures. METHODS: We exposed ovalbumin (OVA)-sensitized A/J mice intratracheally to PM (20 mg/kg), and assayed both AHR and bronchoalveolar lavage (BAL) on days 1, 4, and 7 after PM exposure. Lung gene expression profiling was analyzed in OVA- and PM-challenged mice. RESULTS: Consistent with this murine model of asthma, we observed significant increases in airway responsiveness in OVA-treated mice, with PM exposure inducing significant changes in AHR in both naive mice and OVA-induced asthmatic mice. PM evoked eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of type 1 T helper (T(H)1) cytokines [interferon-gamma, interleukin-6 (IL-6), tumor necrosis factor-alpha] and T(H)2 cytokines (IL-4, IL-5, eotaxin) into murine airways. Furthermore, PM consistently induced expression of genes involved in innate immune responses, chemotaxis, and complement system pathways. CONCLUSION: This study is consistent with emerging epidemiologic evidence and indicates that PM exposure evokes proinflammatory and allergic molecular signatures that may directly contribute to the asthma susceptibility in naive subjects and increased severity in affected asthmatics.

The longitudinal dependence of black carbon concentration on traffic volume in an urban environment.

The purpose of this study was to evaluate the effect of traffic volume on ambient black carbon (BC) concentration in an inner-city neighborhood "hot spot" while accounting for modifying effects of weather and time. Continuous monitoring was conducted for 12 months at the Baltimore Traffic Study site surrounded by major urban streets that together carry over 150,000 vehicles per day. Outdoor BC concentration was measured with an Aethalometer; vehicles were counted pneumatically on two nearby streets. Meteorological data were also obtained. Missing data were imputed and all data were normalized to a 5-min observational interval (n = 105,120). Time-series modeling accounted for autoregressively (AR) correlated errors. This study found that outdoor BC was positively correlated at a statistically significant level with neighborhood-level vehicle counts, which contributed at a rate of 66 +/- 10 (SE) ng/m3 per 100 vehicles every 5 min. Winds from the SW-S-SE quarter were associated with the greatest increases in BC (376-612 ng/m3). These winds would have entrained BC from Baltimore's densely trafficked central business district, as well as a nearby interstate highway. The strong influence of wind direction implicates atmospheric transport processes in determining BC exposure. Dew point, mixing height, wind speed, season, and workday were also statistically significant predictors. Background exposure to BC was estimated to be 905 ng/m3. The optimal, statistically significant representation of BC's autocorrelation was AR([1:6]) x 288 x 2016, where the short-term AR factor (lags 1-6) indicated that BC concentrations are correlated for up to 30 min, and the AR factors for lags 288 and 2016 indicate longer-term autocorrelations at diurnal and weekly cycles, respectively. It was concluded that local exposure to BC from mobile sources is substantially modified by meteorological and temporal conditions, including atmospheric transport processes. BC concentration also demonstrates statistically significant autocorrelation at several time scales.

An approach to checking case-crossover analyses based on equivalence with time-series methods.

The case-crossover design has been increasingly applied to epidemiologic investigations of acute adverse health effects associated with ambient air pollution. The correspondence of the design to that of matched case-control studies makes it inferentially appealing for epidemiologic studies. Case-crossover analyses generally use conditional logistic regression modeling. This technique is equivalent to time-series log-linear regression models when there is a common exposure across individuals, as in air pollution studies. Previous methods for obtaining unbiased estimates for case-crossover analyses have assumed that time-varying risk factors are constant within reference windows. In this paper, we rely on the connection between case-crossover and time-series methods to illustrate model-checking procedures from log-linear model diagnostics for time-stratified case-crossover analyses. Additionally, we compare the relative performance of the time-stratified case-crossover approach to time-series methods under 3 simulated scenarios representing different temporal patterns of daily mortality associated with air pollution in Chicago, Illinois, during 1995 and 1996. Whenever a model-be it time-series or case-crossover-fails to account appropriately for fluctuations in time that confound the exposure, the effect estimate will be biased. It is therefore important to perform model-checking in time-stratified case-crossover analyses rather than assume the estimator is unbiased.

Comparison of arsenic content in pelletized poultry house waste and biosolids fertilizer.

Managers of human biosolids have been incorporating the practice of waste pelletization for use as fertilizer since the mid 1920s, and waste pelletization has recently been embraced by some poultry producers as a way to move nutrients away from saturated agricultural land. However, the presence of arsenic in pelletized poultry house waste (PPHW) resulting from the use of organoarsenical antimicrobial drugs in poultry production raises concerns regarding additional incremental population exposures. Arsenic concentrations were determined in PPHW and pelletized biosolids fertilizer (PBF) samples. Pellets were processed using strong acid microwave digestion and analyzed by graphite furnace atomic absorption spectroscopy. The mean arsenic concentration in PPHW (20.1 ppm) fell within the lower part of the range of previously report arsenic concentrations in unpelletized poultry house waste. Arsenic concentrations in PBF, the source of which is less clear than for PPHW, were approximately a factor of 5 times lower than those in PPHW, with a mean concentration of 4.1 ppm. The pelletization and sale of these biological waste fertilizers present new pathways of exposure to arsenic in consumer populations who would otherwise not come into contact with these wastes. Arsenic exposures in humans resulting from use of these fertilizer pellets should be quantified to avoid potential unintended negative consequences of managing wastes through pelletization.

Microbial and chemical assessment of regions within New Orleans, LA impacted by Hurricane Katrina.

The city of New Orleans, LA was severely impacted by flooding and wind damage following landfall of Hurricane Katrina in August 2005. The city's drinking water infrastructure was severely compromised and massive amounts of sediment were redeposited throughout the flooded region. Thousands of homes were water-damaged resulting in the rapid growth of mold. In September and October 2005 a convenience sample of selected homes, tap water, surface water, and sediment within New Orleans was assessed for mold contamination, microbial contamination, and heavy metal concentrations. At selected sites, indoor mold spore concentrations were compared to outdoor concentrations. The purpose of this study was to conduct a baseline environmental assessment in an effort to identify public health threats caused by wind and flood damage. Surface waters contained high concentrations of bacterial indicators whereas no bacteria were detected in tap water, even from taps containing no chlorine residual. Sediment samples contained concentrations of lead and arsenic similarto pre-Katrina concentrations. Outdoor total spore (sp) concentrations ranged from >6500 to 84 713 sp/m(3). Indoor concentrations ranged from 6142 to 735 123 sp/m(3). For the 13 locations with matched indoor/ outdoor samples, the mean indoor/outdoor spore ratio was 4.11 (ranging from 0.27 to >11.44). Inside 5 of the 13 homes, total spore counts/m(3) exceeded 100 000, with measurements in the moldiest home exceeding 700 000 sp/ m(3). In conclusion, surface waters had high concentrations of bacterial contamination but no bacterial indicators were present in tap water. Sediment samples did not have appreciable increases in lead or arsenic. Flooded homes, however, contained substantial concentrations of mold which could present a public health exposure route to individuals repopulating and restoring the City of New Orleans.

Respiratory effects of inhalation exposure among workers during the clean-up effort at the World Trade Center disaster site.

During December 2001 we conducted a field study of 183 clean-up and recovery workers at the World Trade Center (WTC) disaster site to assess respiratory health effects potentially resulting from their work at the site. On site, we administered a respiratory health questionnaire designed to assess upper respiratory symptoms and lower respiratory symptoms, including cough, phlegm, and wheeze, as well as indices of exposure, including number of days worked at the site and job category. Spirometry was conducted for 175 workers. Sixty-five percent of the workers surveyed arrived at the site without lower respiratory symptoms. Of this group, 34% developed cough, 24% developed phlegm, and 19% developed wheeze. Prevalence rates of these symptoms were related to the number of days spent working at the WTC, but not job category. The mean percentage predicted FEV(1) and FVC were 6% and 5% lower, respectively, for workers who developed new lower respiratory symptoms compared to those who remained symptom free. While the development of new wheeze suggested the presence of airway obstruction, the near-normal distribution of age-adjusted FEV(1)/FVC ratios suggested that the degree of obstruction was mild. The prevalence rates of upper airway symptoms (nasal congestion, sore throat, hoarse throat) exceeded those of lower respiratory symptoms, however, it was not determined whether symptoms pre-dated arrival at the WTC site.

Asbestos exposures to truck drivers during World Trade Center cleanup operations.

This article presents results of asbestos air sampling conducted to assess the exposure to truck drivers working at the World Trade Center site. Sampling consisted of a combination of area and personal monitoring of 49 truck drivers and included optical and electron microscopic analyses. Three sampling periods were conducted: October 1-7, 2001, October 17-26, 2001, and April 13-23, 2002. Area sample locations were selected to estimate airborne concentrations around the perimeter of the site, on top of the pile, and in the pit. Air samples were collected using a 50-mm conductive cowl and a 25-mm mixed cellulose ester filter at flow rates ranging from 0.5-2 L/min. Samples were analyzed using a combination of phase contrast microscopy (PCM) NIOSH method 7400, transmission electron microscopy (TEM) NIOSH method 7402, and the direct method specified under the Asbestos Hazardous Emergency Response Act. Sample times and flow rates were adjusted to prevent overloading while maximizing sample volume. Personal sampling results suggest that asbestos fiber exposures to truck drivers at the site were low. Exposures based on TEM results generally ranged from less than detectable to 0.1 structures per cubic centimeter (s/cm(3)). TEM-based results further indicate that the majority of asbestos fibers were chrysotile and less than 5 microm in length. PCM-based estimates were generally higher than the TEM results. This is likely due to the counting of nonasbestos fibers. This conclusion is supported by the NIOSH 7402 TEM results, which did not detect asbestos fibers longer than 5 micro m. Area sample results were generally less than the personal results (except for the sample collected on top of the rubble pile) and decreased over the course of the cleanup. Our results show low airborne asbestos concentrations and a predominance of short fibers. Given these low concentrations, evidence of short fibers, and the short duration of the exposure (less than 10 months to complete the cleanup), it is likely that truck drivers working at the site are not at an increased risk for asbestos-related disease.