The explosion and collapse of the World Trade Center (WTC) was a catastrophic event that produced an aerosol plume impacting many workers, residents, and commuters during the first few days after 11 September 2001. Three bulk samples of the total settled dust and smoke were collected at weather-protected locations east of the WTC on 16 and 17 September 2001; these samples are representative of the generated material that settled immediately after the explosion and fire and the concurrent collapse of the two structures. We analyzed each sample, not differentiated by particle size, for inorganic and organic composition. In the inorganic analyses, we identified metals, radionuclides, ionic species, asbestos, and inorganic species. In the organic analyses, we identified polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls, polychlorinated dibenzodioxins, polychlorinated dibenzofurans, pesticides, phthalate esters, brominated diphenyl ethers, and other hydrocarbons. Each sample had a basic pH. Asbestos levels ranged from 0.8% to 3.0% of the mass, the PAHs were > 0.1% of the mass, and lead ranged from 101 to 625 microg/g. The content and distribution of material was indicative of a complex mixture of building debris and combustion products in the resulting plume. These three samples were composed primarily of construction materials, soot, paint (leaded and unleaded), and glass fibers (mineral wool and fiberglass). Levels of hydrocarbons indicated unburned or partially burned jet fuel, plastic, cellulose, and other materials that were ignited by the fire. In morphologic analyses we found that a majority of the mass was fibrous and composed of many types of fibers (e.g., mineral wool, fiberglass, asbestos, wood, paper, and cotton). The particles were separated into size classifications by gravimetric and aerodynamic methods. Material < 2.5 microm in aerodynamic diameter was 0.88-1.98% of the total mass. The largest mass concentrations were > 53 microm in diameter. The results obtained from these samples can be used to understand the contact and types of exposures to this unprecedented complex mixture experienced by the surviving residents, commuters, and rescue workers directly affected by the plume from 11 to 12 September and the evaluations of any acute or long-term health effects from resuspendable dust and smoke to the residents, commuters, and local workers, as well as from the materials released after 11 September until the fires were extinguished. Further, these results support the need to have the interior of residences, buildings, and their respective HVAC systems professionally cleaned to reduce long-term residential risks before rehabitation.

The Relationship of Indoor, Outdoor and Personal Air (RIOPA) study was designed to investigate residential indoor, outdoor and personal exposures to several classes of air pollutants, including volatile organic compounds, carbonyls and fine particles (PM 2.5 ). Samples were collected from summer, 1999 to spring, 2001 in Houston (TX), Los Angeles (CA) and Elizabeth (NJ). Indoor, outdoor and personal PM 2.5 samples were collected at 212 nonsmoking residences, 162 of which were sampled twice. Some homes were chosen due to close proximity to ambient sources of one or more target analytes, while others were farther from sources. Median indoor, outdoor and personal PM 2.5 mass concentrations for these three sites were 14.4, 15.5 and 31.4 mg/m 3 , respectively. The contributions of ambient (outdoor) and nonambient sources to indoor and personal concentrations were quantified using a single compartment box model with measured air exchange rate and a random component superposition (RCS) statistical model. The median contribution of ambient sources to indoor PM 2.5 concentrations using the mass balance approach was estimated to be 56% for all study homes (63%, 52% and 33% for California, New Jersey and Texas study homes, respectively). Reasonable variations in model assumptions alter median ambient contributions by less than 20%. The mean of the distribution of ambient contributions across study homes agreed well for the mass balance and RCS models, but the distribution was somewhat broader when calculated using the mass balance model with measured air exchange rates.

The indoor and outdoor concentrations of 30 polycyclic aromatic hydrocarbons (PAHs) were measured in 55 nonsmoking residences in three urban areas during June 1999-May 2000. The data represent the subset of samples collected within the Relationship of Indoor, Outdoor, and Personal Air study (RIOPA). The study collected samples from homes in Los Angeles, CA, Houston, TX, and Elizabeth, NJ. In the outdoor samples, the total PAH concentrations (sigmaPAH) were 4.2-64 ng m(-3) in Los Angeles, 10-160 ng m(-3) in Houston, and 12-110 ng m(-3) in Elizabeth. In the indoor samples, the concentrations of sigmaPAH were 16-220 ng m(-3) in Los Angeles, 21-310 ng m(-3) in Houston, and 22-350 ng m(-3) in Elizabeth. The PAH profiles of low molecular weight PAHs (3-4 rings) in the outdoor samples from the three cities were not significantly different. In contrast, the profiles of 5-7-ring PAHs in thesethree citieswere significantlydifferent, which suggested different dominant PAH sources. The signatures of 5-7-ring PAHs in the indoor samples in each city were similar to the outdoor profiles, which suggested that indoor concentrations of 5-7-ring PAHs were dominated by outdoor sources. Indoor-to-outdoor ratios of the PAH concentrations showed that indoor sources had a significant effect on indoor concentrations of 3-ring PAHs and a smaller effect on 4-ring PAHs and that outdoor sources dominated the indoor concentrations of 5-7-ring PAHs.

The Relationship of Indoor, Outdoor and Personal Air (RIOPA) Study was undertaken to evaluate the contribution of outdoor sources of air toxics, as defined in the 1990 Clean Air Act Amendments, to indoor concentrations and personal exposures. The concentrations of 18 volatile organic compounds (VOCs), 17 carbonyl compounds, and fine particulate matter mass (PM 2.5 ) were measured using 48-h outdoor, indoor and personal air samples collected simultaneously. PM 2.5 mass, as well as several component species (elemental carbon, organic carbon, polyaromatic hydrocarbons and elemental analysis) were also measured; only PM 2.5 mass is reported here. Questionnaires were administered to characterize homes, neighborhoods and personal activities that might affect exposures. The air exchange rate was also measured in each home. Homes in close proximity (o0.5 km) to sources of air toxics were preferentially (2:1) selected for sampling. Approximately 100 non-smoking households in each of Elizabeth, NJ, Houston, TX, and Los Angeles, CA were sampled (100, 105, and 105 respectively) with second visits performed at 84, 93, and 81 homes in each city, respectively. VOC samples were collected at all homes, carbonyls at 90% and PM 2.5 at 60% of the homes. Personal samples were collected from nonsmoking adults and a portion of children living in the target homes. This manuscript provides the RIOPA study design and quality control and assurance data. The results from the RIOPA study can potentially provide information on the influence of ambient sources on indoor air concentrations and exposure for many air toxics and will furnish an opportunity to evaluate exposure models for these compounds.

While there is an awareness of the need to quantify inhalation exposure from showers, the potential for dermal exposure to organic contaminants in showers has not been appreciated or explored. To establish routes of environmental exposure from showers, comparisons of the concentration of chloroform in exhaled breath after a normal shower with municipal tap water were made with those after an inhalation-only exposure. The postexposure chloroform breath concentrations ranged from 6.0-21 micrograms/m3 for normal showers and 2.4 to 10 micrograms/m3 for inhalation-only exposure, while the pre-exposure concentrations were all less than the minimum detection limit of 0.86 micrograms/m3. According to an F-test, the difference between the normal shower and the inhalation-only exposures was considered significant at a probability of p = 0.0001. Based on the difference, the mean internal dose due to dermal exposure was found to be approximately equal to that due to the inhalation exposure. The effect of the showering activities on the concentration of chloroform shower air was examined by comparing air concentrations during a normal shower with the air concentrations obtained when the shower was unoccupied. The F-test showed that there is no significant difference between the two sets of data.

Benzene has been measured throughout the environment and is commonly emitted in several industrial and transportation settings leading to widespread environmental and occupational exposures. Inhalation is the most common exposure route but benzene rapidly penetrates the skin and can contaminant water and food resulting in dermal and ingestion exposures. While less toxic solvents have been substituted for benzene, it still is a component of petroleum products, including gasoline, and is a trace impurity in industrial products resulting in continued sub to low ppm occupational exposures, though higher exposures exist in small, uncontrolled workshops in developing countries. Emissions from gasoline/petrochemical industry are its main sources to the ambient air, but a person’s total inhalation exposure can be elevated from emissions from cigarettes, consumer products and gasoline powered engines/tools stored in garages attached to homes. Air samples are collected in canisters or on adsorbent with subsequent quantification by gas chromatography. Ambient air concentrations vary from sub-ppb range, low ppb, and tens of ppb in rural/suburban, urban, and source impacted areas, respectively. Short-term environmental exposures of ppm occur during vehicle fueling. Indoor air concentrations of tens of ppb occur in microenvironments containing indoor sources. Occupational and environmental exposures have declined where regulations limit benzene in gasoline (<1%) and cigarette smoking has been banned from public and work places. Similar controls should be implemented worldwide to reduce benzene exposure. Biomarkers of benzene used to estimate exposure and risk include: benzene in breath, blood and urine; its urinary metabolites: phenol, t,t-muconic acid (t,tMA) and S-phenylmercapturic acid (sPMA); and blood protein adducts. The biomarker studies suggest benzene environmental exposures are in the sub to low ppb range though non-benzene sources for urinary metabolites, differences in metabolic rates compared to occupational or animal doses, and the presence of polymorphisms need to be considered when evaluating risks from environmental exposures to individuals or potentially susceptible populations.

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ObjectivesRecent studies have explored the potential for swimming pool disinfection by-products (DBPs), which are respiratory irritants, to cause asthma in young children. Here we describe the state of the science on methods for understanding children’s exposure to DBPs and biologics at swimming pools and associations with new-onset childhood asthma and recommend a research agenda to improve our understanding of this issue.Data sourcesA workshop was held in Leuven, Belgium, 21–23 August 2007, to evaluate the literature and to develop a research agenda to better understand children’s exposures in the swimming pool environment and their potential associations with new-onset asthma. Participants, including clinicians, epidemiologists, exposure scientists, pool operations experts, and chemists, reviewed the literature, prepared background summaries, and held extensive discussions on the relevant published studies, knowledge of asthma characterization and exposures at swimming pools, and epidemiologic study designs.SynthesisChildhood swimming and new-onset childhood asthma have clear implications for public health. If attendance at indoor pools increases risk of childhood asthma, then concerns are warranted and action is necessary. If there is no such relationship, these concerns could unnecessarily deter children from indoor swimming and/or compromise water disinfection.ConclusionsCurrent evidence of an association between childhood swimming and new-onset asthma is suggestive but not conclusive. Important data gaps need to be filled, particularly in exposure assessment and characterization of asthma in the very young. Participants recommended that additional evaluations using a multidisciplinary approach are needed to determine whether a clear association exists.