Source proximity and residential outdoor concentrations of PM(2.5), OC, EC, and PAHs.

We examined the effect of proximity to specific mobile, area, and point sources on the residential outdoor concentrations of fine particulate matter PM (PM(2.5)) and several of its particle components. Integrated (48-h) PM(2.5) samples were collected outside non-smoking residences in Elizabeth, NJ, between summer 1999 and spring 2001. Samples were analyzed for PM(2.5) mass, organic and elemental carbon (OC and EC, respectively), trace elements, particle-phase polycyclic aromatic hydrocarbons (p-PAHs), and other important particle species. Information about the proximity of the study homes to potential mobile and area sources of OC, EC, p-PAHs, sulfur (S), and selenium (Se) (including urban interstate highways, local roadways, the Newark International Airport, the Elizabeth seaport, and a nearby refinery in Linden, NJ) were retrieved from a database that included detailed emissions, meteorological, and geographical data for the study area. The dependence of residential outdoor concentrations on source proximity and on various meteorological parameters was then examined for each species by multiple linear regression analysis. As expected, the predicted ambient air concentrations of all particle species (except S, Se) decreased with increasing distance from the sources. Although the enhancement in PM(2.5) and OC levels outside the study homes closest to primary PM sources was modest (e.g., 1.6 and 2.5 times the background levels 37 m from interstate highways), the elevation of EC and p-PAH concentrations was substantial outside the closest study homes (i.e., about 20 times for p-PAHs 37 m from interstate highways and about 14 times for EC 192 m from the refinery in Linden, NJ). The predicted EC concentrations 192 and 500 m from the oil refinery were 22.8 and 3.0 microgC/m(3), compared with an urban background of 1 microgC/m(3). Thus, emissions from this source might dramatically affect EC exposure for residents living in its close proximity.

Toxicokinetics of human exposure to methyl tertiary-butyl ether (MTBE) following short-term controlled exposures.

Methyl tertiary-butyl ether (MTBE) is an oxygenated compound added to gasoline to improve air quality as part of the US Federal Clean Air Act. Due to the increasing and widespread use of MTBE and suspected health effects, a controlled, short-term MTBE inhalation exposure kinetics study was conducted using breath and blood analyses to evaluate the metabolic kinetics of MTBE and its metabolite, tertiary-butyl alcohol (TBA), in the human body. In order to simulate common exposure situations such as gasoline pumping, subjects were exposed to vapors from MTBE in gasoline rather than pure MTBE. Six subjects (three females, three males) were exposed to 1.7 ppm of MTBE generated by vaporizing 15 LV% MTBE gasoline mixture for 15 min. The mean percentage of MTBE absorbed was 65.8 +/- 5.6% following exposures to MTBE. The mean accumulated percentages expired through inhalation for 1 and 8 h after exposure for all subjects were 40.1% and 69.4%, respectively. The three elimination half-lives of the triphasic exponential breath decay curves for the first compartment was 1-4 min, for the second compartment 9-53 min, and for the third compartment 2-8 h. The half-lives data set for the breath second and blood first compartments suggested that the second breath compartment rather than the first breath compartment is associated with a blood compartment. Possible locations for the very short breath half-life observed are in the lungs or mucous membranes. The third compartment calculated for the blood data represent the vessel poor tissues or adipose tissues. A strong correlation between blood MTBE and breath MTBE was found with mean blood-to-breath ratio of 23.5. The peak blood TBA levels occurred after the MTBE peak concentration and reached the highest levels around 2-4 h after exposures. Following the exposures, immediate increases in MTBE urinary excretion rates were observed with lags in the TBA excretion rate. The TBA concentrations reached their highest levels around 6-8 h, and then gradually returned to background levels around 20 h after exposure. Approximately 0.7-1.5% of the inhaled MTBE dose was excreted as unchange urinary MTBE, and 1-3% was excreted as unconjugated urinary TBA within 24 h after exposure.

Controlled human exposure to methyl tertiary butyl ether in gasoline: symptoms, psychophysiologic and neurobehavioral responses of self-reported sensitive persons.

The 1990 Clean Air Act mandated oxygenation of gasoline in regions where carbon monoxide standards were not met. To achieve this standard, methyl tertiary butyl ether (MTBE) was increased to 15% by volume during winter months in many locations. Subsequent to the increase of MTBE in gasoline, commuters reported increases in symptoms such as headache, nausea, and eye, nose, and throat irritation. The present study compared 12 individuals selected based on self-report of symptoms (self-reported sensitives; SRSs) associated with MTBE to 19 controls without self-reported sensitivities. In a double-blind, repeated measures, controlled exposure, subjects were exposed for 15 min to clean air, gasoline, gasoline with 11% MTBE, and gasoline with 15% MTBE. Symptoms, odor ratings, neurobehavioral performance on a task of driving simulation, and psychophysiologic responses (heart and respiration rate, end-tidal CO(2), finger pulse volume, electromyograph, finger temperature) were measured before, during, and immediately after exposure. Relative to controls, SRSs reported significantly more total symptoms when exposed to gasoline with 15% MTBE than when exposed to gasoline with 11% MTBE or to clean air. However, these differences in symptoms were not accompanied by significant differences in neurobehavioral performance or psychophysiologic responses. No significant differences in symptoms or neurobehavioral or psychophysiologic responses were observed when exposure to gasoline with 11% MTBE was compared to clean air or to gasoline. Thus, the present study, although showing increased total symptoms among SRSs when exposed to gasoline with 15% MTBE, did not support a dose-response relationship for MTBE exposure nor the symptom specificity associated with MTBE in epidemiologic studies.

The MTBE air concentrations in the cabin of automobiles while fueling.

Methyl tertiary-butyl ether (MTBE) is the most commonly used oxygenated compound added to gasoline to reduce ambient carbon monoxide levels. Complaints about perceived MTBE exposures and adverse health symptoms have been registered in several states, including New Jersey (NJ). Fueling automobiles is the activity thought to cause the highest environmental MTBE exposures. The current study was conducted to determine the MTBE concentrations inside automobile cabins during fueling, which represents the peak exposure that can occur at full service gasoline service stations, such as those that exist in NJ. Air samples were collected at service stations located on the NJ and PA turnpikes from March 1996 to July 1997 during which the MTBE content in gasoline varied. A bimodal distribution of MTBE concentrations was found in the cabin of the cars while fueling. The median MTBE, benzene and toluene in cabin concentrations were 100, 5.5 and 18 ppb, respectively, with the upper concentrations of the distribution exceeding 1 ppm for MTBE and 0.1 ppm for benzene and toluene. The highest in cabin concentrations occurred in a car that had a malfunctioning vapor recovery system and in a series of cars sampled on an unusually warm, calm winter day when the fuel volatility was high, the evaporation maximal and the dispersion by wind minimal. The in-cabin concentrations were typically higher when the car window was opened during the entire fueling process. Thus, exposure to MTBE during fueling can be reduced by properly maintaining the integrity of the fuel system and keeping the windows closed during fueling.

Determination of methyl tert-butyl ether and tert-butyl alcohol in human urine by high-temperature purge-and-trap gas chromatography-mass spectrometry.

Methyl tert-butyl ether (MTBE) is the oxygenated gasoline additive most widely used in the U.S. to reduce the CO emission from motor vehicles. We developed a method using a high-temperature purge-and-trap procedure coupled with capillary gas chromatography-mass selective detection to determine MTBE and its metabolite, tert-butyl alcohol (TBA), in human urine. Several spiked-urine tests were conducted at different purging temperatures (25, 55, and 90 degrees C). The results indicated that the purging temperature affects the recovery of TBA from urine more than the recovery of MTBE. The mean recoveries of MTBE and TBA in the urine samples by the high temperature (90 degrees C) purge-and-trap gas chromatography-mass spectrometry method at different spike levels were 96.5+/-4.7% and 98.4+/-5.7%, respectively. The method was used to evaluate the urinary levels in a single subject exposed through inhalation to 1 ppm MTBE for 10 min in a controlled-environment facility. Increases in MTBE and TBA urinary excretion rates were clearly evident following the exposure to MTBE. Approximately 0.9% of the amount of MTBE inhaled was excreted unchanged as urinary MTBE, and 2.4% was excreted as urinary TBA within 10 h after exposure. The method developed is a simple, effective, sensitive, and reproducible procedure for evaluating human exposure to MTBE.

Exposure to regular gasoline and ethanol oxyfuel during refueling in Alaska.

Although most people are thought to receive their highest acute exposures to gasoline while refueling, relatively little is actually known about personal, nonoccupational exposures to gasoline during refueling activities. This study was designed to measure exposures associated with the use of an oxygenated fuel under cold conditions in Fairbanks, Alaska. We compared concentrations of gasoline components in the blood and in the personal breathing zone (PBZ) of people who pumped regular unleaded gasoline (referred to as regular gasoline) with concentrations in the blood of those who pumped an oxygenated fuel that was 10% ethanol (E-10). A subset of participants in a wintertime engine performance study provided blood samples before and after pumping gasoline (30 using regular gasoline and 30 using E-10). The biological and environmental samples were analyzed for selected aromatic volatile organic compounds (VOCs) found in gasoline (benzene, ethylbenzene, toluene, m-/p-xylene, and o-xylene); the biological samples were also analyzed for three chemicals not found in gasoline (1,4-dichlorobenzene, chloroform, and styrene). People in our study had significantly higher levels of gasoline components in their blood after pumping gasoline than they had before pumping gasoline. The changes in VOC levels in blood were similar whether the individuals pumped regular gasoline or the E-10 blend. The analysis of PBZ samples indicated that there were also measurable levels of gasoline components in the air during refueling. The VOC levels in PBZ air were similar for the two groups. In this study, we demonstrate that people are briefly exposed to low (ppm and sub-ppm) levels of known carcinogens and other potentially toxic compounds while pumping gasoline, regardless of the type of gasoline used.

Biomarkers of environmental benzene exposure.

Environmental exposures to benzene result in increases in body burden that are reflected in various biomarkers of exposure, including benzene in exhaled breath, benzene in blood and urinary trans-trans-muconic acid and S-phenylmercapturic acid. A review of the literature indicates that these biomarkers can be used to distinguish populations with different levels of exposure (such as smokers from nonsmokers and occupationally exposed from environmentally exposed populations) and to determine differences in metabolism. Biomarkers in humans have shown that the percentage of benzene metabolized by the ring-opening pathway is greater at environmental exposures than that at higher occupational exposures, a trend similar to that found in animal studies. This suggests that the dose-response curve is nonlinear; that potential different metabolic mechanisms exist at high and low doses; and that the validity of a linear extrapolation of adverse effects measured at high doses to a population exposed to lower, environmental levels of benzene is uncertain. Time-series measurements of the biomarker, exhaled breath, were used to evaluate a physiologically based pharmacokinetic (PBPK) model. Biases were identified between the PBPK model predictions and experimental data that were adequately described using an empirical compartmental model. It is suggested that a mapping of the PBPK model to a compartmental model can be done to optimize the parameters in the PBPK model to provide a future framework for developing a population physiologically based pharmacokinetic model.

Measurement of the urinary benzene metabolite trans,trans-muconic acid from benzene exposure in humans.

The concentration of the urinary benzene metabolite trans, trans-muconic acid was measured after exposure to benzene contained in environmental tobacco smoke (ETS). Volunteers were exposed to environmental tobacco smoke at different exposure levels and for different exposure durations. Urine samples were collected preexposure and postexposure for 24 h on exposure days. To determine background levels, urine samples were also collected on three individual days when no exposure to ETS occurred. Urinary muconic acid was elevated following benzene exposure in ETS compared to an individual's background level and can be a useful biomarker in control, characterized studies of sub-parts-per-million (sub-ppm) benzene exposures. However, the use of muconic acid as a bio-marker of benzene exposure at sub-ppm levels in the general population is problematic because of variability in the time between exposure and excretion and in an individual's background excretion rate. Urinary muconic acid associated with benzene in ETS exposure was excreted within 12 h of the exposure. A higher proportion of the benzene dose following environmental exposure in the sub-ppm range was excreted as urinary muconic acid (mean of 25%, range 7.2-58%) than found in either animal or occupational studies at higher benzene doses. The higher proportion of benzene excretion as urinary muconic acid at low benzene exposure indicates that the relationship between exposure and metabolism by the ring opening pathway is nonlinear in humans, and extrapolation from high doses to environmental benzene exposure potentially underestimates health risks mediated by the ring opening metabolic pathway that produces muconic acid, as has been suggested by previous animal data.

Measurement of benzene in human breath associated with an environmental exposure.

The concentration of benzene in breath was measured after exposure to environmental benzene. Five volunteers were exposed to environmental tobacco smoke at different exposure levels and for different exposure durations. The breath samples were collected before, during, and postexposure for up to three hours. Benzene in breath was confirmed as a short-term biomarker of environmental benzene exposure at the sub-ppm level. Less than 10% of the inhaled benzene was expired within three hours following two-hour inhalation exposures, with a greater percentage expired following shorter exposures. An average of 64% percent of the inhaled benzene was absorbed through the lung barrier, with the percentage absorbed decreasing with continued exposure. Benzene biological half-lives of 7.6 and 68 minutes were calculated empirically using a two-compartment model based on the exponential benzene decay curve after correcting the breath concentrations for background breath concentrations. The breath concentration calculated at the end of the exposure by extrapolation of the postexposure breath samples demonstrates a discontinuity with the breath concentration collected during exposure, consistent with equilibrium exchange between blood and breath.

Evaluation of assays for the identification and quantitation of muconic acid, a benzene metabolite in human urine.

Muconic acid (MA) is a urinary metabolite of benzene and has been used as a biomarker of exposure to benzene in humans exposed to levels as low as 1 ppm. We have modified a high-pressure liquid chromatography (HPLC) based assay for urinary MA (Ducos et al., 1990) by the use of a diode array detector. This modification increases the specificity of the HPLC-based assay by identifying false positives. In addition, we have developed a gas chromatography (GC) based assay that uses a flame ionization detector (GC-FID). Both assays identified and quantified MA in human urine at concentrations greater than 40-50 ng/ml. Assay precision was within 10% relative standard deviation for MA concentrations above 90 ng/ml using the HPLC assay and above 40 ng/ml using the GC-FID assay. Quantitative accuracy of the assays was evaluated by determining MA in human urine samples using both methods and also a gas chromatography-mass spectrometry (GC-MS) procedure. Numerical correlation among the three assays was good at MA concentrations above 100 ng/ml.

Exposure to chlorination by-products from hot water uses.

Exposures to chlorination by-products (CBP) within public water supplies are multiroute in water. Cold water is primarily used for ingestion while a mixture of cold water and hot water is used for showering, bathing others, dish washing, etc. These latter two activities result in inhalation and dermal exposure. Heating water was observed to change the concentration of various CBP. An increase in the trihalomethanes (THM) concentrations and a decrease in the haloacetonitriles and halopropanones concentration, though an initial rise in the concentration of dichloropropanone, were observed. The extent of the increase in the THM is dependent on the chlorine residual present. Therefore, estimates of total exposure to CBP from public water supplies need to consider any changes in their concentration with different water uses. The overall THM exposures calculated using the THM concentration in heated water were 50% higher than those calculated using the THM concentration present in cold water. The estimated lifetime cancer risk associated with exposure to THM in water during the shower is therefore underestimated by 50% if the concentration of THM in cold water is used in the risk assessment.