Showing papers by "United States Environmental Protection Agency published in 2003"

Climate Change, Human Impacts, and the Resilience of Coral Reefs

Abstract: The diversity, frequency, and scale of human impacts on coral reefs are increasing to the extent that reefs are threatened globally. Projected increases in carbon dioxide and temperature over the next 50 years exceed the conditions under which coral reefs have flourished over the past half-million years. However, reefs will change rather than disappear entirely, with some species already showing far greater tolerance to climate change and coral bleaching than others. International integration of management strategies that support reef resilience need to be vigorously implemented, and complemented by strong policy decisions to reduce the rate of global warming.

Source partitioning using stable isotopes: coping with too many sources.

Abstract: Stable isotopes are increasingly being used as tracers in environmental studies. One application is to use isotopic ratios to quantitatively determine the proportional contribution of several sources to a mixture, such as the proportion of various pollution sources in a waste stream. In general, the proportional contributions of n+1 different sources can be uniquely determined by the use of n different isotope system tracers (e.g., δ13C, δ15N, δ18O) with linear mixing models based on mass balance equations. Often, however, the number of potential sources exceeds n+1, which prevents finding a unique solution of source proportions. What can be done in these situations? While no definitive solution exists, we propose a method that is informative in determining bounds for the contributions of each source. In this method, all possible combinations of each source contribution (0–100%) are examined in small increments (e.g., 1%). Combinations that sum to the observed mixture isotopic signatures within a small tolerance (e.g., ±0.1‰) are considered to be feasible solutions, from which the frequency and range of potential source contributions can be determined. To avoid misrepresenting the results, users of this procedure should report the distribution of feasible solutions rather than focusing on a single value such as the mean. We applied this method to a variety of environmental studies in which stable isotope tracers were used to quantify the relative magnitude of multiple sources, including (1) plant water use, (2) geochemistry, (3) air pollution, and (4) dietary analysis. This method gives the range of isotopically determined source contributions; additional non-isotopic constraints specific to each study may be used to further restrict this range. The breadth of the isotopically determined ranges depends on the geometry of the mixing space and the similarity of source and mixture isotopic signatures. A sensitivity analysis indicated that the estimated ranges vary only modestly with different choices of source increment and mass balance tolerance parameter values. A computer program (IsoSource) to perform these calculations for user-specified data is available at http://www.epa.gov/wed/pages/models.htm .

Brominated flame retardants: cause for concern?

Abstract: Brominated flame retardants (BFRs) have routinely been added to consumer products for several decades in a successful effort to reduce fire-related injury and property damage. Recently, concern for this emerging class of chemicals has risen because of the occurrence of several classes of BFRs in the environment and in human biota. The widespread production and use of BFRs; strong evidence of increasing contamination of the environment, wildlife, and people; and limited knowledge of potential effects heighten the importance of identifying emerging issues associated with the use of BFRs. In this article, we briefly review scientific issues associated with the use of tetrabromobisphenol A, hexabromocyclododecane, and three commercial mixtures of polybrominated diphenyl ethers and discuss data gaps. Overall, the toxicology database is very limited; the current literature is incomplete and often conflicting. Available data, however, raise concern over the use of certain classes of brominated flame retardants.

Disinfection by-products and other emerging contaminants in drinking water

Abstract: Although drinking-water disinfection by-products (DBPs) have been studied for the last 30 years, significant, new concerns have arisen. These concerns include adverse reproductive and developmental effects recently observed in human populations, concerns that the types of cancer observed in laboratory animals (for regulated DBPs) do not correlate with the cancers observed in human populations (indicating that other DBPs may be important), and concerns arising from human-exposure studies that show that other routes besides ingestion (i.e., inhalation and dermal adsorption) are also significant sources of DBP exposures. In addition, many drinking-water utilities are changing their primary disinfectant from chlorine to alternative disinfectants (e.g., ozone, chlorine dioxide, and chloramines), which generally reduce regulated trihalomethane and haloacetic acid levels, but can increase the levels of other potentially toxicologically important DBPs. For example, results of a new US Nationwide DBP Occurrence Study (discussed in this review) demonstrated that bromo-trihalonitromethanes, iodo-trihalomethanes, dihaloaldehydes, MX (3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone), and brominated forms of MX were formed at higher levels when alternative disinfectants were used to treat drinking water. Specific DBPs of emerging toxicological interest include brominated and iodinated compounds — including bromonitromethanes, iodo-trihalomethanes, iodo-acids, and brominated forms of MX — as well as nitrosodimethylamine (NDMA). In addition to concerns about DBPs, there are also new concerns about the presence of pharmaceuticals, organotins, methyl-tert-butyl ether (MTBE), perchlorate, and algal toxins in drinking water. This article will discuss these drinking-water contaminants of emerging concern and the analytical methods currently being used for their determination.

Traffic Fatalities and Economic Growth

Abstract: Kopits and Cropper examine the impact of income growth on the death rate due to traffic fatalities, as well as on fatalities per motor vehicle and on the motorization rate (vehicles/population) using panel data from 1963-99 for 88 countries. Specifically, they estimate fixed effects models for fatalities/population, vehicles/population, and fatalities/vehicles and use these models to project traffic fatalities and the stock of motor vehicles to 2020. The relationship between motor vehicle fatality rate and per capita income at first increases with per capita income, reaches a peak, and then declines. This is because at low income levels the rate of increase in motor vehicles outpaces the decline in fatalities per motor vehicle. At higher income levels, the reverse occurs. The income level at which per capita traffic fatalities peaks is approximately $8,600 in 1985 international dollars. This is within the range of income at which other externalities, such as air and water pollution, have been found to peak. Projections of future traffic fatalities suggest that the global road death toll will grow by approximately 66 percent between 2000 and 2020. This number, however, reflects divergent rates of change in different parts of the world - a decline in fatalities in high-income countries of approximately 28 percent versus an increase in fatalities of almost 92 percent in China and 147 percent in India. The authors also predict that the fatality rate will rise to approximately 2 per 10,000 persons in developing countries by 2020, while it will fall to less than 1 per 10,000 in high-income countries. This paper - a product of Infrastructure and Environment, Development Research Group - is part of a larger effort in the group to study the externalities associated with motorization.

Environmental technologies at the nanoscale.

Abstract: Nanotechnology could substantially enhance environmental quality and sustainability through pollution prevention, treatment, and remediation.

Resistance and Resilience to Coral Bleaching: Implications for Coral Reef Conservation and Management

Abstract: The massive scale of the 1997–1998 El Nino–associated coral bleaching event underscores the need for strategies to mitigate biodiversity losses resulting from temperature-induced coral mortality. As baseline sea surface temperatures continue to rise, climate change may represent the single greatest threat to coral reefs worldwide. In response, one strategy might be to identify ( 1 ) specific reef areas where natural environmental conditions are likely to result in low or negligible temperature-related bleaching and mortality ( i.e., areas of natural “resistance” to bleaching ) and ( 2 ) reef areas where environmental conditions are likely to result in maximum recovery of reef communities after bleaching mortality has occurred ( i.e., areas of natural community “resilience” ). These “target areas,” where environmental conditions appear to boost resistance and resilience during and after large-scale bleaching events, could then be incorporated into strategic networks of marine protected areas designed to maximize conservation of global coral reef biodiversity. Based on evidence from the literature and systematically compiled observations from researchers in the field, this paper identifies likely environmental correlates of resistance and resilience to coral bleaching, including factors that reduce temperature stress, enhance water movement, decrease light stress, correlate with physiological tolerance, and provide physical or biological enhancement of recovery potential. As a tool for identifying reef areas that are likely to be most robust in the face of continuing climate change and for determining priority areas for reducing direct anthropogenic impacts, this information has important implications for coral reef conservation and management.

PPARα Agonist-Induced Rodent Tumors: Modes of Action and Human Relevance

Abstract: Widely varied chemicals--including certain herbicides, plasticizers, drugs, and natural products--induce peroxisome proliferation in rodent liver and other tissues. This phenomenon is characterized by increases in the volume density and fatty acid oxidation of these organelles, which contain hydrogen peroxide and fatty acid oxidation systems important in lipid metabolism. Research showing that some peroxisome proliferating chemicals are nongenotoxic animal carcinogens stimulated interest in developing mode of action (MOA) information to understand and explain the human relevance of animal tumors associated with these chemicals. Studies have demonstrated that a nuclear hormone receptor implicated in energy homeostasis, designated peroxisome proliferator-activated receptor alpha (PPARalpha), is an obligatory factor in peroxisome proliferation in rodent hepatocytes. This report provides an in-depth analysis of the state of the science on several topics critical to evaluating the relationship between the MOA for PPARalpha agonists and the human relevance of related animal tumors. Topics include a review of existing tumor bioassay data, data from animal and human sources relating to the MOA for PPARalpha agonists in several different tissues, and case studies on the potential human relevance of the animal MOA data. The summary of existing bioassay data discloses substantial species differences in response to peroxisome proliferators in vivo, with rodents more responsive than primates. Among the rat and mouse strains tested, both males and females develop tumors in response to exposure to a wide range of chemicals including DEHP and other phthalates, chlorinated paraffins, chlorinated solvents such as trichloroethylene and perchloroethylene, and certain pesticides and hypolipidemic pharmaceuticals. MOA data from three different rodent tissues--rat and mouse liver, rat pancreas, and rat testis--lead to several different postulated MOAs, some beginning with PPARalpha activation as a causal first step. For example, studies in rodent liver identified seven "key events," including three "causal events"--activation of PPARalpha, perturbation of cell proliferation and apoptosis, and selective clonal expansion--and a series of associative events involving peroxisome proliferation, hepatocyte oxidative stress, and Kupffer-cell-mediated events. Similar in-depth analysis for rat Leydig-cell tumors (LCTs) posits one MOA that begins with PPARalpha activation in the liver, but two possible pathways, one secondary to liver induction and the other direct inhibition of testicular testosterone biosynthesis. For this tumor, both proposed pathways involve changes in the metabolism and quantity of related hormones and hormone precursors. Key events in the postulated MOA for the third tumor type, pancreatic acinar-cell tumors (PACTs) in rats, also begin with PPARalpha activation in the liver, followed by changes in bile synthesis and composition. Using the new human relevance framework (HRF) (see companion article), case studies involving PPARalpha-related tumors in each of these three tissues produced a range of outcomes, depending partly on the quality and quantity of MOA data available from laboratory animals and related information from human data sources.

Polybrominated diphenyl ethers (PBDEs) in U.S. mothers' milk.

Abstract: No previous reports exist on polybrominated diphenyl ether (PBDE) congeners in human milk from individual U.S. mothers. This article on PBDEs is an extension of our previous studies on concentrations of dioxins, dibenzofurans, polychlorinated biphenyls, and other chlorinated organic compounds in human milk in a number of countries. PBDE commercial products are used as flame retardants in flexible polyurethane foam (penta-BDE), in acrylonitrile-butadiene-styrene resins (octa-BDE), and in high-impact polystyrene resins (deca-BDE). Their use is permitted in the United States but is banned in some European countries because of presumed toxicity, demonstrated persistence, and bioaccumulation. Different commercial products can be found in various consumer products such as television sets, computers, computer monitors and printers, carpets, and upholstery. Analyses of human levels of these compounds suggest low but rising levels in European human milk, which may have peaked, at least in Sweden, in the late 1990s. Very few data exist on levels of PBDEs in humans in the United States, and none from milk from individual nursing mothers. To address this issue, we analyzed 47 individual milk samples from nursing mothers, 20-41 years of age, from a milk bank in Austin, Texas, and a community women's health clinic in Dallas, Texas. Up to 13 PBDE congeners were measured. The concentrations of the sum of PBDE congeners varied from 6.2 to 419 ng/g (or parts per billion) lipid, with a median of 34 ng/g and a mean of 73.9 ng/g lipid. The PBDE levels in breast milk from Texas were similar to levels found in U.S. blood and adipose tissue lipid from California and Indiana and are 10-100 times greater than human tissue levels in Europe. Their detection in breast milk raises concern for potential toxicity to nursing infants, given the persistence and bioaccumulative nature of some of the PBDE congeners. These results indicate a need for more detailed investigation of the levels of PBDE in people and food, as well as determining if animal fat in food is the major route of exposure of the general U.S. population. Other routes of intake may also be significant.

Source–sink balance and carbon allocation below ground in plants exposed to ozone

Abstract: Contents Summary 213 I. Introduction 213 II. Source–sink model: carbohydrate signaling 214 III. Effect of ozone on above-ground sources and sinks 216 IV. Decreased allocation below ground 218 V. Carbon flux to soils 220 VI. Soil food web 223 VII. Summary, conclusions and future research 223 Acknowledgements 223 References 223 Summary The role of tropospheric ozone in altering plant growth and development has been the subject of thousands of publications over the last several decades. Still, there is limited understanding regarding the possible effects of ozone on soil processes. In this review, the effects of ozone are discussed using the flow of carbon from the atmosphere, through the plant to soils, and back to the atmosphere as a framework. A conceptual model based on carbohydrate signaling is used to illustrate physiological changes in response to ozone, and to discuss possible feedbacks that may occur. Despite past emphasis on above-ground effects, ozone has the potential to alter below-ground processes and hence ecosystem characteristics in ways that are not currently being considered.

Geodesic Discrete Global Grid Systems

Abstract: In recent years, a number of data structures for global geo-referenced data sets have been proposed based on regular, multi-resolution partitions of polyhedra. We present a survey of the most promising of such systems, which we call Geodesic Discrete Global Grid Systems (Geodesic DGGSs). We show that Geodesic DGGS alternatives can be constructed by specifying five substantially independent design choices: a base regular polyhedron, a fixed orientation of the base regular polyhedron relative to the Earth, a hierarchical spatial partitioning method defined symmetrically on a face (or set of faces) of the base regular polyhedron, a method for transforming that planar partition to the corresponding spherical/ellipsoidal surface, and a method for assigning point representations to grid cells. The majority of systems surveyed are based on the icosahedron, use an aperture 4 triangle or hexagon partition, and are either created directly on the surface of the sphere or by using an equal-area transformation. An exa...

A framework for human relevance analysis of information on carcinogenic modes of action.

Abstract: The human relevance framework (HRF) outlines a four-part process, beginning with data on the mode of action (MOA) in laboratory animals, for evaluating the human relevance of animal tumors. Drawing on U.S. EPA and IPCS proposals for animal MOA analysis, the HRF expands those analyses to include a systematic evaluation of comparability, or lack of comparability, between the postulated animal MOA and related information from human data sources. The HRF evolved through a series of case studies representing several different MOAs. HRF analyses produced divergent outcomes, some leading to complete risk assessment and others discontinuing the process, according to the data available from animal and human sources. Two case examples call for complete risk assessments. One is the default: When data are insufficient to confidently postulate a MOA for test animals, the animal tumor data are presumed to be relevant for risk assessment and a complete risk assessment is necessary. The other is the product of a data-based finding that the animal MOA is relevant to humans. For the specific MOA and endpoint combinations studied for this article, full risk assessments are necessary for potentially relevant MOAs involving cytotoxicity and cell proliferation in animals and humans (Case Study 6, chloroform) and formation of urinary-tract calculi (Case Study 7, melamine). In other circumstances, when data-based findings for the chemical and endpoint combination studied indicate that the tumor-related animal MOA is unlikely to have a human counterpart, there is little reason to continue the risk assessment for that combination. Similarly, when qualitative considerations identify MOAs specific to the test species or quantitative considerations indicate that the animal MOA is unlikely to occur in humans, such hazard findings are generally conclusive and further risk assessment is not necessary for the endpoint-MOA combination under study. Case examples include a tumor-related protein specific to test animals (Case Study 3, d-limonene), the tumor consequences of hormone suppression typical of laboratory animals but not humans (Case Study 4, atrazine), and chemical-related enhanced hormone clearance rates in animals relative to humans (Case Study 5, phenobarbital). The human relevance analysis is highly specific for the chemical-MOA-tissue-endpoint combination under analysis in any particular case: different tissues, different endpoints, or alternative MOAs for a given chemical may result in different human relevance findings. By providing a systematic approach to using MOA data, the HRF offers a new tool for the scientific community's overall effort to enhance the predictive power, reliability and transparency of cancer risk assessment.

Effects of the androgenic growth promoter 17‐β‐trenbolone on fecundity and reproductive endocrinology of the fathead minnow

Abstract: Trenbolone acetate is a synthetic steroid that is extensively used in the United States as a growth promoter in beef cattle. The acetate is administered to livestock via slow-release implants; some is converted by the animal to 17-beta-trenbolone, a relatively potent androgen receptor agonist in mammalian systems. Recent studies indicate that excreted 17-beta-trenbolone is comparatively stable in animal waste, suggesting the potential for exposure to aquatic animals via direct discharge, runoff, or both. However, little is known concerning the toxicity of trenbolone to fish. Our goal was to assess the effects of 17-beta-trenbolone on reproductive endocrinology of the fathead minnow (Pimephales promelas). An in vitro competitive binding study with the fathead minnow androgen receptor demonstrated that 17-beta-trenbolone had a higher affinity for the receptor than that of the endogenous ligand, testosterone. Male and female fish were exposed for 21 d to nominal (target) concentrations of 17-beta-trenbolone ranging from 0.005 to 50 microg/L. Fecundity of the fish was significantly reduced by exposure to measured test concentrations > or = 0.027 microg/ L. The 17-beta-trenbolone was clearly androgenic in vivo at these concentrations, as evidenced by the de novo production in females of dorsal (nuptial) tubercles, structures normally present only on the heads of mature males. Plasma steroid (testosterone and beta-estradiol) and vitellogenin concentrations in the females all were significantly reduced by exposure to 17-beta-trenbolone. The 17-beta-trenbolone also altered reproductive physiology of male fathead minnows, albeit at concentrations much higher than those producing effects in females. Males exposed to 17-beta-trenbolone at 41 microg/L (measured) exhibited decreased plasma concentrations of 11-ketotestosterone and increased concentrations of beta-estradiol and vitellogenin. Overall, our studies indicate that 17-beta-trenbolone is a potent androgen and reproductive toxicant in fish. Given the widespread use of trenbolone acetate as a growth promoter, and relative stability of its metabolites in animal wastes, further studies are warranted to assess potential ecological risk.

Urbanization effects on tree growth in the vicinity of New York City

Abstract: Plants in urban ecosystems are exposed to many pollutants and higher temperatures, CO2 and nitrogen deposition than plants in rural areas. Although each factor has a detrimental or beneficial influence on plant growth, the net effect of all factors and the key driving variables are unknown. We grew the same cottonwood clone in urban and rural sites and found that urban plant biomass was double that of rural sites. Using soil transplants, nutrient budgets, chamber experiments and multiple regression analyses, we show that soils, temperature, CO2, nutrient deposition, urban air pollutants and microclimatic variables could not account for increased growth in the city. Rather, higher rural ozone (O3) exposures reduced growth at rural sites. Urban precursors fuel the reactions of O3 formation, but NO(x) scavenging reactions resulted in lower cumulative urban O3 exposures compared to agricultural and forested sites throughout the northeastern USA. Our study shows the overriding effect of O3 despite a diversity of altered environmental factors, reveals 'footprints' of lower cumulative urban O3 exposures amidst a background of higher regional exposures, and shows a greater adverse effect of urban pollutant emissions beyond the urban core.

Are Bt crops safe

Abstract: The US EPA's analysis of Bt crops finds that they pose no significant risk to the environment or to human health.

Endocrine-disrupting effects of cattle feedlot effluent on an aquatic sentinel species, the fathead minnow.

Abstract: Over the last decade, research has examined the endocrine-disrupting action of various environmental pollutants, including hormones, pharmaceuticals, and surfactants, in sewage treatment plant effluent. Responding to the growth of concentrated animal feeding operations (CAFOs) and the pollutants present in their wastewater (e.g., nutrients, pharmaceuticals, and hormones), the U.S. Environmental Protection Agency developed a new rule that tightens the regulation of CAFOs. In this study, we collected wild fathead minnows (Pimephales promelas) exposed to feedlot effluent (FLE) and observed significant alterations in their reproductive biology. Male fish were demasculinized (having lower testicular testosterone synthesis, altered head morphometrics, and smaller testis size). Defeminization of females, as evidenced by a decreased estrogen:androgen ratio of in vitro steroid hormone synthesis, was also documented. We did not observe characteristics in either male or female fish indicative of exposure to environmental estrogens. Using cells transfected with the human androgen receptor, we detected potent androgenic responses from the FLE. Taken together, our morphologic, endocrinologic, and in vitro gene activation assay data suggest two hypotheses: a) there are potent androgenic substance(s) in the FLE, and/or b) there is a complex mixture of androgenic and estrogenic substances that alter the hypothalamic-pituitary-gonadal axis, inhibiting the release of gonadotropin-releasing hormone or gonadotropins. This is the first study demonstrating that the endocrine and reproductive systems of wild fish can be adversely affected by FLE. Future studies are needed to further investigate the effects of agricultural runoff and to identify the biologically active agents, whether natural or pharmaceutical in origin.

Health effects and risk assessment of arsenic

Abstract: Humans can be exposed to arsenic (As) through the intake of air, food and water. Although food is usually the major source of As exposure for people, most adverse effects are seen after As exposure from drinking water. The two main reasons for this situation are that most food arsenicals are organic and have little or no toxicity, and in many cases, As exposures from drinking water sources are to the more toxic inorganic form and occur at relatively high doses, e.g., hundreds of micrograms per day. In various parts of the world, As in drinking water is associated with such effects as gastroenteritis, neurological manifestations, vascular changes, diabetes and cancers (bladder, lung, liver, kidney and prostate). After reviewing the As database, the U.S. Environmental Protection Agency promulgated a maximum contaminant level for As in drinking water of 10 micro g/L.

Cradle-to-cradle stewardship of drugs for minimizing their environmental disposition while promoting human health. I. Rationale for and avenues toward a green pharmacy.

Abstract: Since the 1980s, the occurrence of pharmaceuticals and personal care products (PPCPs) as trace environmental pollutants, originating primarily from consumer use and actions rather than manufacturer effluents, continues to become more firmly established. Although PPCPs typically have been identified in surface and ground waters, some are also undoubtedly associated with solid phases such as suspended particulates, sediments, and sewage sludges, despite their relatively high affinity for water. Often amenable to degradation, their continual introduction to waste-receiving waters results from their widespread, continuous, combined use by individuals and domestic animals, giving PPCPs a "pseudo-persistence" in the environment. Little is known about the environmental or human health hazards that might be posed by chronic, subtherapeutic levels of these bioactive substances or their transformation products. The continually growing, worldwide importance of freshwater resources, however, underscores the need for ensuring that any aggregate or cumulative impacts on (or from) water supplies are minimized. Despite the paucity of effects data from long-term, simultaneous exposure at low doses to multiple xenobiotics (particularly non-target-organism exposure to PPCPs), a wide range of proactive actions could be implemented to reduce or minimize the introduction of PPCPs to the environment. Most of these actions fall under what could be envisioned as a holistic stewardship program--overseen by the health care industry and consumers alike. Significantly, such a stewardship program would benefit not just the environment; additional, collateral benefits could automatically accrue, including reducing consumers' medication expenses and improving patient health and consumer safety. In this article, the first of a two-part mini-monograph describing the "green pharmacy," I focus initially on the background behind the imperative for an ecologically oriented stewardship program for PPCPs. I then present a broad spectrum of possible source control/reduction actions, controlled largely by the health care industry, that could minimize the disposition of PPCPs to the environment. This two-part mini-monograph attempts to capture cohesively for the first time the wide spectrum of actions available for minimizing the release of PPCPs to the environment. A major objective is to generate an active dialog or debate across the many disciplines that must become actively involved to design and implement a successful approach to life-cycle stewardship of PPCPs.

Blood Lead Concentration and Delayed Puberty in Girls

Abstract: Background Environmental lead exposure has been linked to alterations in growth and endocrine function. It is not known whether such exposure affects pubertal development. Methods We analyzed the relations between blood lead concentration and pubertal development among girls (defined as females 8 to 18 years of age) who were enrolled in a cross-sectional study (the third National Health and Nutrition Examination Survey) in which race was self-reported or proxy-reported: 600 were non-Hispanic white, 805 were non-Hispanic African-American, and 781 were Mexican-American girls. Puberty was measured on the basis of the age at menarche and Tanner stage for pubic-hair and breast development. Results Geometric mean lead concentrations were less than 3 μg per deciliter (0.144 μmol per liter) in all three groups. As compared with concentrations of 1 μg per deciliter (0.048 μmol per liter), lead concentrations of 3 μg per deciliter were associated with decreased height (P<0.001), after adjustment for age, race, and ...