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PubMed2001

Malignant mesothelioma and asbestos exposure among auto mechanics: appraisal of scientific evidence.

In 1986 the U.S. Environmental Protection Agency (EPA) issued an official guideline on the prevention of asbestos disease among auto mechanics. In the EPA guideline, malignant mesothelioma was listed as a consequence of exposure to asbestos fibers from brake linings and clutch facings among auto mechanics. EPA formulated its 1986 opinion by relying solely on a few outdated case reports and not on epidemiologic studies. A review of the literature indicates that there are six epidemiologic studies providing relevant information on malignant mesothelioma among auto mechanics. Three of the six studies had already been published by 1986, the year in which EPA issued its guideline. The results of the six studies were remarkably consistent in that all six studies reported no increased risk of malignant mesothelioma among auto mechanics. The relative risks reported in the six studies ranged from 0.62 to 1.00. Based on a meta-analysis of the combined data of all six studies consisting of approximately 1500 malignant mesothelioma cases, the mesothelioma relative risk for auto mechanics is 0.90 (95% confidence interval 0.66-1.23). An application of Hill's causation criteria to epidemiologic data of malignant mesothelioma among auto mechanics clearly demonstrates that auto mechanics do not have an increased risk of malignant mesothelioma as a result of exposure to asbestos fibers from brake linings and clutch facings. However, in spite of the scientific evidence, EPA has not modified or revised its 1986 guideline. Occupational regulatory policies and guidelines, when based on proper scientific evidence, are invaluable and can prevent avoidable diseases in workers or other exposed individuals in the general public. On the other hand, it is the regulators' responsibility to develop, modify, and revise policies and guidelines in accordance with the most relevant and the latest scientific data. In this instance EPA as a regulator has not fulfilled its responsibility of providing the most accurate and up-to-date information to the workers or the general public.

Asbestos↗
PubMed1995

Associations between criteria air pollutants and asthma.

The evidence that asthma is increasing in prevalence is becoming increasingly compelling. This trend has been demonstrated not only in the United States, but also in the United Kingdom, New Zealand, Australia, and several other Western countries. In the United States, the increase is largest in the group under 18 years of age. There is mounting evidence that certain environmental air pollutants are involved in exacerbating asthma. This is based primarily on epidemiologic studies and more recent clinical studies. The U.S. Clean Air Act of 1970 provides special consideration to the class of outdoor air pollutants referred to as criteria pollutants, including O3, sulfur dioxide (SO2), particulate matter (PM), NOx, CO, and Pb. Standards for these pollutants are set by the U.S. Environmental Protection Agency with particular concern for populations at risk. Current evidence suggests that asthmatics are more sensitive to the effects of O3, SO2, PM, and NO2, and are therefore at risk. High SO2 and particulate concentrations have been associated with short-term increases in morbidity and mortality in the general population during dramatic air pollution episodes in the past. Controlled exposure studies have clearly shown that asthmatics are sensitive to low levels of SO2. Exercising asthmatics exposed to SO2 develop bronchoconstriction within minutes, even at levels of 0.25 ppm. Responses are modified by air temperature, humidity, and exercise level. Recent epidemiologic studies have suggested that exposure to PM is strongly associated with morbidity and mortality in the general population and that hospital admissions for bronchitis and asthma were associated with PM10 levels. In controlled clinical studies, asthmatics appear to be no more reactive to aerosols than healthy subjects. Consequently, it is difficult to attribute the increased mortality observed in epidemiologic studies to specific effects demonstrated in controlled human studies. Epidemiologic studies of hospital admissions for asthma have implicated O3 as contributing to the exacerbation of asthma; however, most study designs could not separate the O3 effects from the concomitant effects of acid aerosols and SO2. Controlled human clinical studies have suggested that asthmatics have similar changes in spirometry and airway reactivity in response to O3 exposure compared to healthy adults. However, a possible role of O3 in worsening atopic asthma has recently been suggested in studies combining allergen challenge following exposure to O3. Attempts at identification of factors that predispose asthmatics to responsiveness to NO2 has produced inconsistent results and requires further investigation. In summary, asthmatics have been shown to be a sensitive subpopulation relative to several of the criteria pollutants. Further research linking epidemiologic, clinical, and toxicologic approaches is required to better understand and characterize the risk of exposing asthmatics to these pollutants.

Adolescent↗
PubMed1995

Reconsideration of the genetic risk assessment for ethylene oxide exposures.

The US Environmental Protection Agency (EPA) developed a genetic risk assessment model for exposures to ethylene oxide utilizing data on the induction of reciprocal translocations in male germ cells [Rhomberg et al. 1990]. This particular approach served as a reasonable initial attempt, albeit somewhat limited with regard to endpoint and only partially attentive to the mechanisms of induction of genetic alterations and the behavior of chromosomes during meiosis. The present paper discusses the scientific basis for a reassessment of the EPA model, providing data and hypotheses related to effective dose to the target cells and shape of the dose-response relationship at low doses, and dose rates. While the present genetic risk assessment approach is discussed in terms of ethylene oxide, it would be applicable to most mutagenic chemicals. The outcome of the discussion is that the genetic risk for exposed males from reciprocal translocation induction will be negligible at low doses since the dose-response curve is likely to be a function of the square of the dose. In addition, the proportion of genetically unbalanced live born offspring in humans arising from reciprocal translocation carriers is less than 10% of the frequency formed through meiotic segregation and fertilization for such carriers. Simply from a consideration of mechanism--namely, the very high probability of DNA repair prior to the next S-phase for a resting oocyte--it would be predicted that there would be a very low to negligible frequency of translocations in female germ cells from ethylene oxide exposure. It is further stressed that additional components of a genetic risk model require a consideration of all germ cell stages in the male, and the inclusion of calculations for point and deletion mutations. Some indications of likely response are presented with these points in mind.

Animals↗
PubMed2000

Variability in pesticides residues--the US experience.

The evolution of US Environmental Protection Agency's (EPA) process for estimating potential health risks from pesticide residues in or on food is examined in light of changes in US Legislation and the variability of residue data and assumptions used to estimate dietary exposure. In the 86 years since enactment of the Insecticide Act, pesticide laws have become progressively more health-based. Passage of the 1996 Food Quality Protection Act (FQPA) requires EPA to place particular emphasis on assessing potential risk from pesticides to infants and children. Primary factors affecting the actual pesticide residues in food include frequency of application, percentage of crop treated, and the interval from treatment to harvest. Primary factors affecting the estimated pesticide residues in food include the source of the residue data, calculation techniques for non-detected residues, and the availability of data reflecting post-harvest treatments. Risk assessors must thoroughly consider these factors when assessing dietary risk to pesticides. Risk managers will need to consider these factors as a means of mitigating dietary risk from pesticides.

Adult↗
PubMedDate not supplied

Implementation of EPA's Worker Protection Standard training for agricultural laborers: an evaluation using North Carolina data.

The US Environmental Protection Agency has promulgated a Worker Protection Standard which requires that farmworkers receive pesticide safety training. The implementation of these regulations has not been evaluated. Using data collected through personal interviews with 270 Hispanic farmworkers recruited from 35 labor sites in an eight-county area, the authors analyzed the extent to which farmworkers received pesticide safety training, characteristics of the training, and variations in knowledge and safety behavior. Approximately a third of the farmworkers reported having ever received information or training on pesticide safety, and 25.6% reported having received training in the year in which they were interviewed. Workers with H2A visas were significantly more likely to have received training than workers without these visas. The training received varied in location, duration, and language. Most included the use of a video, as well as verbal presentation, and most included printed materials. However, few workers knew the ways in which they could be exposed to pesticides or reported using any method to protect themselves from pesticide exposure.

Adult↗
PubMed2006

VCCEP pilot: progress on evaluating children's risks and data needs.

The Voluntary Children's Chemical Evaluation Program (VCCEP) is designed to provide information to the public on children's potential health risks associated with chemical exposures. The key question of the VCCEP is whether the potential hazards, exposures, and risks to children have been adequately characterized, and, if not, what additional data are necessary. To answer this question, manufacturers or importers of 23 chemicals were asked by the U. S. Environmental Protection Agency (U.S. EPA) to sponsor their chemicals in the first tier of a pilot program. These chemicals were selected for evaluation because they have been found as contaminants in human tissue or fluids (adipose tissue, blood, breath, breast milk, or urine); food and water children may eat and drink; or air children may breathe (including residential or school air). Under the VCCEP framework, sponsoring companies agree to prepare Tier 1 hazard, exposure, and risk assessments on the individual chemicals, and identify the need for additional data. These assessment documents are submitted to the U.S. EPA and subsequently undergo review by experts in an independent peer consultation meeting that is open to the public. Following this peer consultation process, the U.S. EPA reviews each submission and makes a data-needs determination, which may include requesting further data collection or generation by the sponsor. Sponsoring companies then decide whether to volunteer for the next tier and collect or generate the requested data. The purpose of this article is to describe the VCCEP process and to review and present the key findings from the first set of chemicals that have been fully or partially evaluated under the pilot program (vinylidene chloride, decabromodiphenyl ether, pentabromodiphenyl ether, octabromodiphenyl ether, acetone, methyl ethyl ketone, decane, undecane, and dodecane). Specifically, we provide a brief summary of the sponsors' submissions, the peer consultation panels' discussions, and the U.S. EPA's data-needs decisions. Although we do not attempt to conduct independent analyses of the underlying data, we do identify a number of common themes that have emerged during implementation of the pilot program and discuss several key issues that could become important in the future. The information presented here should be useful for various parties interested in the progress of the VCCEP and the results of the initial (Tier 1) children's assessments.

Acetone↗
PubMed2004

Use of the laboratory rat as a model in endocrine disruptor screening and testing.

The screening and testing program the US Environmental Protection Agency (EPA) is currently developing to detect endocrine-disrupting chemicals (EDCs) is described. EDCs have been shown to alter the following activities: hypothalamic-pituitary-gonadal (HPG) function; estrogen, androgen, and thyroid hormone synthesis; and androgen and estrogen receptor-mediated effects in mammals and other animals. The value and limitations of mammalian in vivo assays are described that involve the use of the laboratory rat, the EPA Endocrine Disruptor Screening and Testing Advisory Committee species of choice. The discussion includes the evaluation of high-priority chemicals positive in the Tier 1 Screening (T1S) battery, and of subsequent testing in the Tier 2 (T2) battery, with additional short-term screening assays proposed for use in T1.5 to eliminate any uncertainty about T1S results. Descriptions include the in vivo uterotropic assay, which detects estrogens and antiestrogens; the pubertal female assay, which assesses steroidogenesis, antithyroid activity, antiestrogenicity, and HPG function; and the Hershberger assay, which detects the weight of androgen-dependent tissues in castrate-immature-male rats (antiandrogens). Of the several alternative mammalian in vivo assays proposed, a short-term pubertal male rat assay appears most promising for inclusion in T1 or T1.5. An additional in utero-lactational screening protocol is being evaluated, but appears to be better suited for T1.5 or T2 due to the size, complexity, and duration of the assay. The adult intact male assay, also proposed as an alternative for T1, attempts to identify EDCs in a hormonal battery, but has limited value as a screen due to lack of sensitivity and specificity. For Tier 2 testing, the number of endocrine-sensitive endpoints and offspring (F1) examined in multigenerational tests must be thoughtfully expanded for EDCs on a mode-of-action-specific basis, with consideration given to tailoring T2 based on the results of T1S.

Animals↗
PubMed1985

Airborne fiber control in buildings during asbestos material removal by amended water methodology.

Removal of friable asbestos-containing material can cause high levels of airborne contamination. The potential efficacy of control methods recommended by the Environmental Protection Agency (EPA) was evaluated by examination of 503 air samples obtained in 40 removal projects in a number of locations. The EPA methodology with amended water for fiber emission control was utilized on all of the observed removal projects. The projects were also considered to be well controlled and the study cannot be considered representative of common work practices. The EPA amended water methodology, when effectively utilized and administered, can provide a high degree of contamination control. Mean fiber levels in the work area in this study (1.1 f/cm3) were well below those of dry removal (38.9 f/cm3) and control by application by untreated water (28.6 f/cm3). Airborne contamination was higher during bagging debris (3.8 f/cm3) than during material removal from structural surfaces. The range of fiber levels during removal was 0.0 to 37.0 f/cm3 and fibers were detected from initial barrier construction through final cleaning. Contamination was also occasionally detected outside work area containment barriers. Air sampling produced 0.0 counts in areas of obvious contamination by settled dust and debris. Control methodologies, respiratory protection, and decontamination are discussed.

Air Pollutants↗
PubMed1995

222Rn in water: a study of two sample collection methods, effects of mailing samples, and temporal variation of concentrations in North Carolina groundwater.

The U.S. Environmental Protection Agency has proposed a drinking water standard for 222Rn in public water supplies. When promulgated, operators of public water supplies will be required to determine water 222Rn concentrations. Most likely, water samples will be collected and mailed to laboratories for analyses. Additionally, it is probable that homeowners will test private well water in a similar manner by collecting water samples and mailing them to a laboratory for 222Rn analyses. In anticipation of these actions, this study was conducted to evaluate two methods of water sample collection and to evaluate the potential losses of 222Rn from water samples mailed to a laboratory. Thirdly, temporal variations in 222Rn concentrations in several groundwater supplies in North Carolina were examined. Water supplies at four sites in eastern North Carolina and five sites in western North Carolina were sampled over a 7-mo period beginning in the fall of 1993 and continuing through the spring of 1994. Samples were analyzed using a liquid scintillation method. This study showed that a "slow-flow" method is not only suitable for sample collection, but may be the preferable method for water sample collection since slow-flow collection resulted in less 222Rn loss than was observed during syringe collection, i.e., the water 222Rn concentrations in samples collected by the slow-flow method were generally higher. Further, based on this study, mailing water samples to a laboratory for analysis should not have a substantial effect on the measured 222Rn concentrations. Consequently, water samples can be collected by the slow-flow method by water supply operators, as well as homeowners, and mailed to laboratories for 222Rn analyses with reasonable assurance that the samples have not suffered significant 222Rn loss. Temporal variations in water 222Rn concentrations were observed in this study. One factor complicating the study of temporal variations in 222Rn concentrations was the striking influence that inconstant water usage and inadequate well purging prior to sample collection had on 222Rn loss from the water.

Evaluation Studies as Topic↗
PubMed2002

Xenoendocrine disrupters-tiered screening and testing: filling key data gaps.

The US Environmental Protection Agency (EPA) is developing a screening and testing program for endocrine disrupting chemicals (EDCs) to detect alterations of hypothalamic-pituitary-gonadal (HPG) function, estrogen (ER), androgen (AR) and thyroid hormone synthesis and AR and ER receptor-mediated effects in mammals and other animals. High priority chemicals would be evaluated in the Tier 1 Screening (T1S) battery and chemicals positive in T1S would then be tested (Tier 2). T1S includes in vitro ER and AR receptor binding and/or gene expression, an assessment of steroidogenesis and mammalian (rat) and nonmammalian in vivo assays (Table 1). In vivo, the uterotropic assay detects estrogens and antiestrogens, while steroidogenesis, antithyroid activity, (anti)estrogenicity and HPG function are assessed in a 'Pubertal Female Assay'. (Anti-) androgens are detected in the Hershberger Assay (weight of AR-dependent tissues in castrate-immature-male rats). Fish and amphibian assays also are being developed. The fathead minnow assay can identify EDCs displaying several mechanisms of concern, including AR and ER receptor agonists and antagonists and inhibitors of steroid hormone synthesis. An amphibian metamorphosis assay is being developed to detect thyroid-active substances. Several alternative mammalian in vivo assays have been proposed. Of these, a short-term pubertal male rat assay appears most promising. An in utero-lactational screening protocol also is being evaluated. For Tier 2, the numbers of endocrine sensitive endpoints and offspring (F1) examined in multigenerational tests need to be expanded for EDCs. Consideration should be given to tailoring T2, based on the results of T1S. Tier 1 and 2 also should examine relevant mixtures of EDCs. Toxicants that induce malformations in AR-dependent tissues produce cumulative effects even when two chemicals act via different mechanisms of action.

Animals↗
PubMed2002

Ambient level volatile organic compound (VOC) monitoring using solid adsorbents--recent US EPA studies.

Ambient air spiked with 1-10 ppbv concentrations of 41 toxic volatile organic compounds (VOCs) listed in US Environmental Protection Agency (EPA) Compendium Method TO-14A was monitored using solid sorbents for sample collection and a Varian Saturn 2000 ion trap mass spectrometer for analysis. The adsorbent was a combination of graphitic carbon and a Carboxen-type carbon molecular sieve. The method detection limits (MDLs) for 11 samples were typically 0.5 parts per billion by volume (ppbv) and lower except for bromomethane and chloromethane, both of which exhibited breakthrough. Thirty-day sample storage on the sorbents resulted in less than a 20% change for most compounds, and water management was required for humid samples to avoid major anomalous decreases in response during analyses. The adsorbent-based system, a system using canister-based monitoring, and a semi-continuous automated GC/MS (autoGC) monitoring system with a Tenax GR/Carbotrap B/Carbosieve S-III adsorbent preconcentrator were compared using spiked ozone concentrations as a variable. In this comparison, the target compounds included a number of n-aldehydes as well as those listed in TO-14A. The effects of ozone on the TO-14A compounds were relatively minor with the exception of negative artifacts noted for styrene and 1,1,2,2-tetrachloroethane. However, a small, systematic decrease in response was evident for a number of aromatic VOCs and 1,1,2,2-tetrachloroethane when ozone was increased from 50 to 300 ppbv. Method averages for multiple runs under the same conditions were typically within +0.25 ppbv of their mean for most compounds. For n-aldehydes, strong positive artifacts using the autoGC preconcentrator and strong negative artifacts for the canister-based and carbon sorbent approaches caused major disagreement among methods. These artifacts were mostly eliminated by using MnO2 ozone scrubbers, although loss of the n-aldehydes for all methods occurred after a single sample collection of 1 h duration, apparently due to the interaction of the n-aldehydes and products of the O3, MnO2 reaction on the scrubber.

Adsorption↗
PubMed1991

The Los Angeles TEAM Study: personal exposures, indoor-outdoor air concentrations, and breath concentrations of 25 volatile organic compounds.

The U.S. Environmental Protection Agency and the California Air Resources Board studied the exposures of 51 residents of Los Angeles, California, to 25 volatile organic chemicals (VOCs) in air and drinking water in 1987. A major goal of the study was to measure personal, indoor, and outdoor air concentrations, and breath concentrations of VOCs in persons living in households that had previously been measured in 1984. Other goals were to confirm the marked day-night and seasonal differences observed in 1984; to determine room-to-room variability within homes; to determine source emission rates by measuring air exchange rates in each home; and to extend the coverage of chemicals by employing additional sampling and analysis methods. A total of 51 homes were visited in February of 1987, and 43 of these were revisited in July of 1987. The results confirmed previous TEAM Study findings of higher personal and indoor air concentrations than outdoor concentrations of all prevalent chemicals (except carbon tetrachloride); higher personal, indoor, and outdoor air concentrations in winter than in summer; and (in winter only) higher outdoor concentrations at night than in the daytime. New findings included the following: (1) room-to-room variability of 12-hour average concentrations was very small, indicating that a single monitor may be adequate for estimating indoor concentrations over this time span; (2) "whole-house" source emission rates were relatively constant during both seasons, with higher rates for odorous chemicals such as p-dichlorobenzene and limonene (often used in room air fresheners) than for other classes of chemicals; (3) breath concentrations measured during morning and evening were similar for most participants, suggesting the suitability of breath measurements for estimating exposure in the home; (4) limited data obtained on two additional chemicals-toluene and methylene chloride-indicated that both were prevalent at fairly high concentrations and that indoor air concentrations exceeded outdoor concentrations by a factor of about three.

Adolescent↗
PubMed2006

An approach for developing a national estimate of waterborne disease due to drinking water and a national estimate model application.

In this paper, the US Environmental Protection Agency (EPA) presents an approach and a national estimate of drinking water related endemic acute gastrointestinal illness (AGI) that uses information from epidemiologic studies. There have been a limited number of epidemiologic studies that have measured waterborne disease occurrence in the United States. For this analysis, we assume that certain unknown incidence of AGI in each public drinking water system is due to drinking water and that a statistical distribution of the different incidence rates for the population served by each system can be estimated to inform a mean national estimate of AGI illness due to drinking water. Data from public water systems suggest that the incidence rate of AGI due to drinking water may vary by several orders of magnitude. In addition, data from epidemiologic studies show AGI incidence due to drinking water ranging from essentially none (or less than the study detection level) to a rate of 0.26 cases per person-year. Considering these two perspectives collectively, and associated uncertainties, EPA has developed an analytical approach and model for generating a national estimate of annual AGI illness due to drinking water. EPA developed a national estimate of waterborne disease to address, in part, the 1996 Safe Drinking Water Act Amendments. The national estimate uses best available science, but also recognizes gaps in the data to support some of the model assumptions and uncertainties in the estimate. Based on the model presented, EPA estimates a mean incidence of AGI attributable to drinking water of 0.06 cases per year (with a 95% credible interval of 0.02-0.12). The mean estimate represents approximately 8.5% of cases of AGI illness due to all causes among the population served by community water systems. The estimated incidence translates to 16.4 million cases/year among the same population. The estimate illustrates the potential usefulness and challenges of the approach, and provides a focus for discussions of data needs and future study designs. Areas of major uncertainty that currently limit the usefulness of the approach are discussed in the context of the estimate analysis.

Communicable Diseases↗
PubMed1997

EPA's neurotoxicity risk assessment guidelines.

The proposed Neurotoxicity Risk Assessment Guidelines (U.S. EPA, 1995c Fed. Reg. 60(192), 52032-52056) of the U.S. Environmental Protection Agency (EPA) were the subject of a workshop at the 1997 Meeting of the Society of Toxicology. The workshop considered the role of guidelines in the risk assessment process, the primary features, scientific basis, and implications of the guidelines for EPA program offices, as well as for industrial neurotoxicologists from the perspectives of both pesticides and toxic substances regulation. The U.S. National Academy of Sciences (NAS, 1983, Risk Assessment in the Federal Government: Managing the Process) established a framework for distinguishing risk management from risk assessment, the latter being the result of integrating hazard identification, hazard characterization, and exposure assessment data. The guidelines are intended to establish operating principles that will be used when examining data in a risk assessment context. The proposed neurotoxicity risk assessment guidelines provide a conceptual framework for deciding whether or not a chemically induced effect can be considered to be evidence of neurotoxicity. Topics in the proposed guidelines include structural and functional effects, dose-response and -duration considerations, and relationships between effects. Among the issues that must be considered are the multiplicity of chemical effects, the levels of biological organization in the nervous system, and the tests, measurements, and protocols used. Judgment of the adversity of an effect depends heavily on the amount and types of data available. The attribution of a chemically induced effect to an action on the nervous system depends on several factors such as the quality of the study, the nature of the outcome, dose-response and time-response relationships, and the possible involvement of nonneural factors. The guidelines will also serve as a reference for those conducting neurotoxicity testing, as well as establish a consistent approach to neurotoxicity risk assessment by regulators. Extending this approach through international harmonization would be advantageous to the development of products for a worldwide market. Thus, both risk assessors and regulated industries have a large stake in the guidelines to provide a framework that will lead to accurate risk assessment decisions.

Data Collection↗
PubMed2003

Estimated emission reductions from California's enhanced Smog Check program.

The U.S. Environmental Protection Agency requires that states evaluate the effectiveness of their vehicle emissions inspection and maintenance (I/M) programs. This study demonstrates an evaluation approach that estimates mass emission reductions over time and includes the effect of I/M on vehicle deterioration. It includes a quantitative assessment of benefits from pre-inspection maintenance and repairs and accounts for the selection bias effect that occurs when intermittent high emitters are tested. We report estimates of one-cycle emission benefits of California's Enhanced Smog Check program, ca. 1999. Program benefits equivalent to metric tons per day of prevented emissions were calculated with a "bottom-up" approach that combined average per vehicle reductions in mass emission rates (g/gal) with average per vehicle activity, resolved by model year. Accelerated simulation mode test data from the statewide vehicle information database (VID) and from roadside Smog Check testing were used to determine 2-yr emission profiles of vehicles passing through Smog Check and infer emission profiles that would occur without Smog Check. The number of vehicles participating in Smog Check was also determined from the VID. We estimate that in 1999 Smog Check reduced tailpipe emissions of HC, CO, and NO(x) by 97, 1690, and 81 t/d, respectively. These correspond to 26, 34, and 14% of the HC, CO, and NO(x) that would have been emitted by vehicles in the absence of Smog Check. These estimates are highly sensitive to assumptions about vehicle deterioration in the absence of Smog Check. Considering the estimated uncertainty in these assumptions yields a range for calculated benefits: 46-128 t/d of HC, 860-2200 t/d of CO, and 60-91 t/d of NO(x). Repair of vehicles that failed an initial, official Smog Check appears to be the most important mechanism of emission reductions, but pre-inspection maintenance and repair also contributed substantially. Benefits from removal of nonpassing vehicles accounted for a small portion of total benefits. In 1999, more than 90% of all HC and CO benefits and over 80% of all NO(x) benefits were attributed to vehicles more than 10 years old, even though such vehicles represented only half of those tested in the program.

Air Pollution↗
PubMed2000

Lessons learned in applying the U.S. EPA proposed cancer guidelines to specific compounds.

An expert panel was convened to evaluate the U.S. Environmental Protection Agency's "Proposed Guidelines for Carcinogen Risk Assessment" through their application to data sets for chloroform (CHCl3) and dichloroacetic acid (DCA). The panel also commented on perceived strengths and limitations encountered in applying the guidelines to these specific compounds. This latter aspect of the panel's activities is the focus of this perspective. The panel was very enthusiastic about the evolution of these proposed guidelines, which represent a major step forward from earlier EPA guidance on cancer-risk assessment. These new guidelines provide the latitude to consider diverse scientific data and allow considerable flexibility in dose-response assessments, depending on the chemical's mode of action. They serve as a very useful template for incorporating state-of-the-art science into carcinogen risk assessments. In addition, the new guidelines promote harmonization of methodologies for cancer- and noncancer-risk assessments. While new guidance on the qualitative decisions ensuing from the determination of mode of action is relatively straightforward, the description of the quantitative implementation of various risk-assessment options requires additional development. Specific areas needing clarification include: (1) the decision criteria for judging the adequacy of the weight of evidence for any particular mode of action; (2) the role of mode of action in guiding development of toxicokinetic, biologically based or case-specific models; (3) the manner in which mode of action and other technical considerations provide guidance on margin-of-exposure calculations; (4) the relative roles of the risk manager versus the risk assessor in evaluating the margin of exposure; and (5 ) the influence of mode of action in harmonizing cancer and noncancer risk assessment methodologies. These points are elaborated as recommendations for improvements to any revisions. In general, the incorporation of examples of quantitative assessments for specific chemicals would strengthen the guidelines. Clearly, any revisions should retain the emphasis present in these draft guidelines on flexibility in the use of scientific information with individual compounds, while simultaneously improving the description of the processes by which these mode-of-action data are organized and interpreted.

Animals↗
PubMedDate not supplied

Health effects of tropospheric ozone: review of recent research findings and their implications to ambient air quality standards.

The U.S. Environmental Protection Agency (EPA) Administrator proposed (on August 3, 1992) to retain the current National Ambient Air Quality Standard (NAAQS) for ozone (O3) on the basis of data assembled in a draft Criteria Document (1986) and its Addendum (1988) which, together with a draft Staff Paper (1988), received public comment and review comments by the EPA's Clean Air Scientific Advisory Committee (CASAC). This paper summarizes and discusses research findings presented since 1988 which, based on the author's experience as a Chairman of CASAC, are most relevant to the promulgation of a primary (health based) NAAQS for O3. These newer findings include substantial evidence from controlled chamber exposure studies and field studies in natural settings that the current NAAQS contains no margin of safety against short-term effects that the EPA has considered to be adverse. They also include evidence from epidemiologic studies that current ambient exposures are associated with reduced baseline lung function, exacerbation of asthma and premature mortality, as well as evidence from chronic animal exposure studies at concentrations within current ambient peak levels that indicate progressive and persistent lung function and structural abnormalities. The current NAAQS, if retained, may therefore also be inadequate to protect the public from effects resulting from chronic exposure to O3.

Adult↗
PubMedDate not supplied

Interlaboratory evaluation of an off-line supercritical fluid extraction/infrared spectrometric method for determination of petroleum hydrocarbons in solid matrixes.

A collaborative study was conducted, with 14 laboratories participating, to determine the method accuracy and precision of the proposed U.S. Environmental Protection Agency Methods 3560 and 8440. These methods involve the extraction of petroleum hydrocarbons from solid matrixes with supercritical carbon dioxide at 340 atm and 80 degrees C for 30 min (dynamic), collection of the extracted materials in tetrachloroethene (Method 3560), and analysis of the extracts by infrared (IR) spectrometry (Method 8440). The study design was based on the AOAC blind replicate design with balanced replicates. The study samples consisted of 4 solid matrixes that had petroleum hydrocarbon contents ranging from 614 to 32,600 mg/kg. Each of the 4 matrixes was extracted in triplicate, and the extracts were analyzed with 2 different IR spectrometers. In addition, each of the participating laboratories extracted a sample of unspiked clay soil, the same clay soil spiked with corn oil and reference oil at 1000 mg/kg each, and the same clay soil wetted to 30% water content and spiked with motor oil at 10,000 mg/kg (the latter 3 samples were extracted only once). Results indicated that the overall method accuracy for concentrations ranging from 614 to 32,600 mg/kg was 82.9%; the mean recoveries of petroleum hydrocarbons for each of the 4 solid matrixes ranged from 77.9 to 107% for analyses performed with the Perkin-Elmer Fourier transform IR spectrometer and from 75.9 to 101% for analyses performed with the Buck-Scientific IR spectrometer; the differences between the 2 instruments on a sample-by-sample basis were less than 17% for the total petroleum hydrocarbon determinations. The interlaboratory method precisions (RSDR) appeared to be matrix-dependent and ranged from 17.3 to 45.4% for analyses performed with the Perkin-Elmer Fourier transform IR spectrometer and from 16.7 to 47.9% for the Buck-Scientific IR spectrometer. The intralaboratory method precisions (RSDr) appeared to be less matrix-dependent and ranged from 11.5 to 17.0% for analyses performed with the Perkin-Elmer FTIR spectrometer and from 11.1 to 18.2% for the Buck-Scientific IR spectrometer. Method accuracy and precision data are also presented for the 5 laboratories that used Isco supercritical fluid extraction systems and for the 7 laboratories that used vessels with volumes of 3.5 mL or less with different supercritical fluid extraction systems.

Aluminum Silicates↗