Human symptom responses to bioeffluents, short-chain carbonyls/acids, and long-chain carbonyls in a simulated aircraft cabin environment.

Occupants of aircraft have reported an array of symptoms related to general discomfort and irritation. Volatile organic compounds (VOCs) have been suggested to contribute to the reported symptoms. VOCs are from products used, bioeffluents from people and oxidation reaction products. Thirty-six healthy, young female subjects rated symptoms and environmental quality during an eight-hour exposure to groups of compounds often present in aircraft: (i) long-chain carbonyls, (ii) simulated bioeffluents, and (iii) short-chain carbonyls/organic acids. Statistically more symptoms were identified for the simulated bioeffluents and, to a lesser extent, short-chain carbonyls/organic acids compared to a control condition, although they remained in the acceptable range. There were three temporal patterns in the environmental quality and symptom reports: (i) an adaptive response (immediate increases followed by a decline); (ii) an apparent physiological effect (increases one to three hours into the exposure that remained elevated); and (iii) no statistical differences in reported environmental quality or symptom severity compared to the control air conditions. Typical concentrations found in aircraft can cause transitory symptoms in healthy individuals questioning the adequacy of current standards. Understanding the effects on individuals sensitive to air pollutants and methods to remove the compounds causing the greatest symptom responses are needed.

Functional group characterization of indoor, outdoor, and personal PM: results from RIOPA.

UNLABELLED: Fourier transform infrared (FTIR) spectra of outdoor, indoor, and personal fine particulate matter (PM(2.5)) samples were collected during the Relationship of Indoor, Outdoor, and Personal Air (RIOPA) study. FTIR spectroscopy provides functional group information about the entire PM(2.5) sample without any chemical preparation. It is particularly important to characterizing the poorly understood organic fraction of PM(2.5). To our knowledge this is the first time that FTIR spectroscopy has been applied to a PM(2.5) exposure study. The results were used to chemically characterize indoor air and personal exposure. Sulfate was strongest in outdoor samples, which is consistent with the generally accepted understanding that sulfate is of outdoor origin. Absorbances attributed to soil dust were also seen in many outdoor and some indoor and personal samples. Inorganic nitrate absorbances were a common feature of many California and some New Jersey samples. Carbonyl absorbances showed substantial variation in strength, number of peaks, and wave number shift between samples, indicating variability in composition and sources. Absorbances attributed to aliphatic hydrocarbon and amide functional groups were enhanced in many personal and indoor samples, which suggested the influence of indoor sources in these homes. We speculate that meat cooking is one possible source of particulate amides. PRACTICAL IMPLICATIONS: To our knowledge this is the first time that FTIR spectroscopy has been used to characterize the composition of indoor and personal PM(2.5). The presence of sulfate, nitrate, ammonium, soil dust and a number of organic functional groups are all detected in one analysis on filter samples without extraction or other sample preparation. Differences between indoor and outdoor spectra are used to identify spectral features due to indoor-generated PM(2.5). Particularly interesting are the much larger aliphatic absorbances, shifts in carbonyl absorbances, and occasional small amide absorbances found in indoor and personal spectra but rarely in outdoor spectra. These observations are important because organics make up a large portion of PM(2.5) mass and their composition and properties are poorly characterized. The properties and behavior of organic compounds in airborne particles are often predicted based on their functional group composition. This analysis begins the development of a better understanding of the functional group composition of indoor and personal PM(2.5) and how it differs from that of outdoor PM(2.5). Eventually this will lead to an improved understanding of the properties, behavior and effects of PM(2.5) of indoor and outdoor origin.

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.

Penetration of evaporative emissions into a home from an M85-fueled vehicle parked in an attached garage.

The use of both oxygenated fuels in carbon monoxide (CO) nonattainment areas and reformulated gasoline in ozone nonattainment areas has been mandated by the 1990 Clean Air Act Amendments. Methanol has been proposed as an alternative fuel for CO nonattainment areas. Its use will potentially increase indoor methanol inhalation exposure resulting from the evaporation of methanol vapor from methanol-fueled vehicles parked in residential garages. Indoor air concentrations of methanol, benzene, and toluene were measured in a residential home with an attached garage. The effects of vehicle emission control devices (charcoal canister hose connection); home heating, ventilation, and air conditioning (HVAC) fans; ambient air, garage, and fuel tank temperatures; and wind speed were examined. The disconnection of the charcoal canister hose, which simulates a spent evaporative emission control device, resulted in elevated benzene, toluene, and methanol concentrations in the garage and attached home. Higher fuel tank temperatures resulted in higher benzene and toluene concentrations in the garage, but not methanol. The concentrations for all compounds in the garage and concentrations of benzene and toluene in the adjacent room were lower when the HVAC fan was on than when it was off, while the concentrations of all three compounds in the rest of the house were higher, although these differences were not statistically significant. Thus, the portion of the population that parks cars in garages attached to homes will experience increased methanol exposures if methanol is used as an automotive fuel.

Evaluation of biomarkers of environmental exposures: urinary haloacetic acids associated with ingestion of chlorinated drinking water.

A study was conducted to determine if DCAA and TCAA urinary excretion rates are valid biomarkers of chronic ingestion exposure to these disinfection by-products of chlorination of drinking water. Entire first morning urine voids, time-of-visit urine samples, and tap water samples were collected from 47 female subjects. In addition, a 48-h recall questionnaire was administered to determine the amounts and types of liquids ingested by each subject as well as other exposures that could lead to DCAA and TCAA urinary excretion. The TCAA excretion rate for the first morning urine samples was significantly correlated with the estimated 48-h TCAA ingestion exposure for 25 subjects whose ingestion exposures primarily occurred at home, while the DCAA excretion rate was not correlated with the DCAA ingestion exposure. Thus, urinary TCAA appears to be a valid biomarker of chronic ingestion exposure to TCAA from chlorinated water, while urinary DCAA is not. It is proposed that the difference in the biological half-lives between these two compounds is the rationale for this finding. The biological half-life of TCAA is longer than successive exposure intervals; thus TCAA accumulates until it reaches a steady state. The half-life of DCAA is shorter than successive exposure intervals; thus DCAA is almost completely metabolized following an exposure and is eliminated from the body. This study suggests that biological half-life, exposure interval, and sample collection interval should be considered in selecting biomarkers and designing studies to validate them.

The effect of dust lead control on blood lead in toddlers: a randomized trial.

BACKGROUND: Contaminated household dust is believed to be a major source of exposure for most children with elevated blood lead levels. To determine if a vigorous dust clean-up effort would reduce this exposure we conducted a randomized controlled field trial. METHODS: We randomized 113 urban children between the ages of 6 and 36 months: 56 children to a lead dust intervention composed of maternal education and biweekly assistance with household cleaning and 57 children to a control group. Household cleaning was done by two trained lay workers who focused their efforts on wet mopping of floors, damp-sponging of walls and horizontal surfaces, and vacuuming with a high-efficiency particle accumulating vacuum. Household dust lead levels, child blood lead levels, and maternal knowledge of lead poisoning and sources of exposure were measured before and after the intervention. RESULTS: Ninety-nine children were successfully followed for 12 +/- 3 months: 46 children in the lead group and 53 children in the control group. Age and blood lead were similar in the two groups at baseline and averaged 20 months and 12.0 micrograms/dL, respectively. Blood lead fell 17% in the intervention group and did not change among controls. Household dust and dust lead measures also fell significantly in the intervention group. Children in homes cleaned 20 or more times throughout the year had an average blood lead reduction of 34%. CONCLUSIONS: Regular home cleaning, accompanied by maternal education, is a safe and partially effective intervention that should be recommended for the large majority of lead-exposed children for whom, unfortunately, removal to lead-safe housing is not an option.

Exposure estimates to disinfection by-products of chlorinated drinking water.

Exposure to disinfection by-products (DBPs) of drinking water is multiroute and occurs in households serviced by municipal water treatment facilities that disinfect the water as a necessary step to halt the spread of waterborne infectious diseases. Biomarkers of the two most abundant groups of DBPs of chlorination, exhaled breath levels of trihalomethanes (THMs) and urinary levels of two haloacetic acids, were compared to exposure estimates calculated from in-home tap water concentrations and responses to a questionnaire related to water usage. Background THM breath concentrations were uniformly low. Strong relationships were identified between the THM breath concentrations collected after a shower and both the THM water concentration and the THM exposure from a shower, after adjusting for the postshower delay time in collecting the breath sample. Urinary haloacetic acid excretion rates were not correlated to water concentrations. Urinary trichloroacetic acid excretion rates were correlated with ingestion exposure, and that correlation was stronger in a subset of individuals who consumed beverages primarily within their home where the concentration measurements were made. No correlation was observed between an average 48-hr exposure estimate and the urinary dichloroacetic acid excretion rate, presumably because of its short biological half-life. Valid biomarkers were identified for DBP exposures, but the time between the exposure and sample collection should be considered to account for different metabolic rates among the DBPs. Further, using water concentration as an exposure estimate can introduce misclassification of exposure for DBPs whose primary route is ingestion due to the great variability in the amount of water ingested across a population.

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.

Urinary mercury levels before and after amalgam restoration.

Urinary mercury levels and excretion rates were measured to determine the effect of dental amalgam restoration on the mercury body burden. No consistent increase in urinary mercury concentrations was found among subjects who had a single restoration, but a continuously increasing statistically significant (P < 0.05) trend, that was 33% above background levels, was detected between 9 and 12 days after restoration, in the subject with four restorations in a single day. The current findings suggested that even though amalgam restorations can cause an increase in mercury body burden, the elevation above background levels is small and thus the risks associated with the use of this material are considered minimal for the general population.

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.

A distributed parameter physiologically-based pharmacokinetic model for dermal and inhalation exposure to volatile organic compounds.

Estimates of dermal dose from exposures to toxic chemicals are typically derived using models that assume instantaneous establishment of steady-state dermal mass flux. However, dermal absorption theory indicates that this assumption is invalid for short-term exposures to volatile organic chemicals (VOCs). A generalized distributed parameter physiologically-based pharmacokinetic model (DP-PBPK), which describes unsteady state dermal mass flux via a partial differential equation (Fickian diffusion), has been developed for inhalation and dermal absorption of VOCs. In the present study, the DP-PBPK model has been parameterized for chloroform, and compared with two simpler PBPK models of chloroform. The latter are lumped parameter models, employing ordinary differential equations, that do not account for the dermal absorption time lag associated with the accumulation of permeant chemical in tissue represented by permeability coefficients. All three models were evaluated by comparing simulated post-exposure exhaled breath concentration profiles with measured concentrations following environmental chloroform exposures. The DP-PBPK model predicted a time-lag in the exhaled breath concentration profile, consistent with the experimental data. The DP-PBPK model also predicted significant volatilization of chloroform, for a simulated dermal exposure scenario. The end-exposure dermal dose predicted by the DP-PBPK model is similar to that predicted by the EPA recommended method for short-term exposures, and is significantly greater than the end-exposure dose predicted by the lumped parameter models. However, the net dermal dose predicted by the DP-PBPK model is substantially less than that predicted by the EPA method, due to the post-exposure volatilization predicted by the DP-PBPK model. Moreover, the net dermal dose of chloroform predicted by all three models was nearly the same, even though the lumped parameter models did not predict substantial volatilization.

Ingestion, inhalation, and dermal exposures to chloroform and trichloroethene from tap water.

Individuals are exposed to volatile compounds present in tap water by ingestion, inhalation, and dermal absorption. Traditional risk assessments for water often only consider ingestion exposure to toxic chemicals, even though showering has been shown to increase the body burden of certain chemicals due to inhalation exposure and dermal absorption. We collected and analyzed time-series samples of expired alveolar breath to evaluate changes in concentrations of volatile organic compounds being expired, which reflects the rate of change in the bloodstream due to expiration, metabolism, and absorption into tissues. Analysis of chloroform and trichloethene in expired breath, compounds regulated in water, was also used to determine uptake from tap water by each route (inhalation, ingestion, or absorption). Each route of exposure contributed to the total exposure of these compounds from daily water use. Further, the ingestion dose was completely metabolized before entering the bloodstream, whereas the dose from the other routes was dispersed throughout the body. Thus, differences in potential biologically effective doses depend on route, target organ, and whether the contaminant or metabolite is the biologically active agent.

Exposure to volatile organic compounds in the passenger compartment of automobiles during periods of normal and malfunctioning operation.

In-vehicle exposures to selected gasoline-derived volatile organic compounds (VOCs) and formaldehyde were examined on 113 commutes through suburban New Jersey and on 33 New Jersey/New York commutes using measurements taken in two vehicles driven in tandem during 1991-1992. Overall median exposures to VOCs were lowest on the suburban commute, slightly higher on the New Jersey Turnpike, and highest in transit through the Lincoln Tunnel. Median in-vehicle concentrations of benzene, ethylbenzene, m- and p-xylene, and o-xylene were 14 microg/m3, 6.8 microg/m3, 36 microg/m3, and 15 microg/m3, respectively. For a motorist who commutes 93.2 min daily (6.5% of the day), this corresponds to 12.1%, 10.8%, 14.9%, and 14.7% of the total daily exposures to these compounds. One vehicle, with a carbureted engine, developed malfunctions which caused gasoline emissions within the engine compartment during driving. Resultant gasoline-derived VOC concentrations in this vehicle measured much higher than in the properly maintained, fuel-injected vehicle, particularly for the low ventilation extreme. The highest in-vehicle benzene concentration measured during these malfunctions was 45.2 microg/m3. The air concentration in the vehicle driven in tandem was a factor of 25 less (1.8 microg/m3). A motorist who drives for the average daily period of 93.2 min/day in this malfunctioning automobile will have a benzene exposure of 2.8 (microg/m3)day, compared to 0.1 (microg/m3)day in the properly functioning vehicle.

Relationship between summertime ambient ozone levels and emergency department visits for asthma in central New Jersey.

The 5-year retrospective study of the association between temperature and emergency department (ED) visits for asthma with mean ambient ozone levels between 10:00 and 15:00 was conducted in central New Jersey during the summer months. An association was identified in each of the years (1986-1990). Between 8 and 34% of the total variance in ED visits for asthma was explained by the two environmental variables in the step-wise multiple regression analysis. ED visits occurred 28% more frequently when the mean ozone levels were > 0.06 ppm than when they were < 0.06 ppm. This result was statistically significant in a covariance analysis. An evaluation of the effects of ozone on asthmatics reported in the literature was completed to determine if, as proposed by Bates, the results from different types of studies were coherent among the health metrics. A consistency in the magnitude of reported effects and the time lag between exposure and response for four different health indices (symptom reports, decrements in expiratory flow, ED visits, and hospital admissions) was identified and indicates a coherence between ozone and respiratory response to ozone exposure. This supports a proposition that ozone adversely affects asthmatics at levels below the current U.S. standard.

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.

The effect of ozone associated with summertime photochemical smog on the frequency of asthma visits to hospital emergency departments.

A retrospective study using ambient ozone, temperature, and other environmental variables and their effect on the frequency of hospital visits for asthma was conducted in New Jersey, an area that often exceeds the allowable national standard for ozone. Data on emergency department visits for asthma, bronchitis, and finger wounds (a nonrespiratory control) were analyzed for the period May through August for 1988 and 1989. Asthma visits were correlated with temperature while the correlation between asthma visits and ozone concentration was nonsignificant. However, when temperature was controlled for in a multiple regression analysis, a highly significant relationship between asthma visits and ozone concentration was identified. Between 13 and 15% of the variability of the asthma visits was explained in the regression model by temperature and ambient ozone levels. This association, when compared to similar studies in Canada, shows the contribution of ozone to asthma admissions to be stronger in areas with higher ozone concentrations. Thus, among regions with periodic accumulations of ozone in the ambient atmosphere, an exposure-response relationship may be discernible. This supports the need to attain air quality standards for ozone to protect individuals in the general population from the adverse health effects caused by ambient ozone exposure.