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Humans are potentially exposed to phthalate esters (PEs) through ingestion, inhalation, and dermal contact. Studies quantifying exposure to PEs include 'biomarker studies' and 'indirect studies.' Biomarker studies use measurements of PE metabolites in urine to back-calculate exposure to the parent diester, while indirect studies use the concentration of the PE in each medium of exposure and the rate of intake of that medium to quantify intake of the PE. In this review, exposure estimates from biomarker and indirect studies are compiled and compared for seven PEs to determine if there are regional differences and if there is a preferred approach. The indirect and biomarker methods generally agree with each other within an order of magnitude and discrepancies are explained by difficulties in accounting for use of consumer products, uncertainty concerning absorption, regional differences, and temporal changes. No single method is preferred for estimating intake of all PEs; it is suggested that biomarker estimates be used for low molecular weight PEs for which it is difficult to quantify all sources of exposure and either indirect or biomarker methods be used for higher molecular weight PEs. The indirect methods are useful in identifying sources of exposure while the biomarker methods quantify exposure. [ABSTRACT FROM AUTHOR]

The most commonly detected environmental metabolites of nonylphenol ethoxylates (NPE) are nonylphenol monoethoxylate (NPE1), nonylphenol diethoxylate (NPE2), nonylphenol ether carboxylates (NPEC), and nonylphenol (NP). Since NPEC have relatively low toxicity, the most relevant NPE metabolites for conducting an aggregate hazard assessment are NP, NPE1, and NPE2. Recent studies support the validity of the U.S. Environmental Protection Agency (2005) chronic water quality criteria (WQC) for NP in freshwater and saltwater environments; thus, these criteria were used as reference values in the aggregate hazard assessment. The toxic equivalency approach was used to assess the aggregate hazard of NP, NPE1, and NPE2. A review of relevant studies indicated that the toxic equivalency factor (TEF) for NPE1 and NPE2 approximated 0.37, which supported the use of the more conservative TEF value of 0.50 used by Environment Canada (2001) for NPE1 and NPE2. The interaction of toxicities between NP, NPE1, and NPE2 is assumed to be additive based on a review of the current literature and the shared mechanism of action of these compounds. The data support previous findings that there is a low likelihood that aggregate NP-equivalent concentrations of NPE and its metabolites in U.S. waters will exceed the national chronic WQC for NP. [ABSTRACT FROM AUTHOR]

This study was conducted to develop a statistical understanding of exposures to C8- and C9-alkylphenol ethoxylates (APEO) and their metabolites (APEM) in U.S. surface waters. Concentrations of APEO/APEM (all analytes) in freshwater have been reported by 19 investigations over the past 15 years. Only limited data are available for sediments and marine ecosystems. Based on the frequency of detection in surface waters, 67% of all analytes were below their detection limits. Although maximum reported concentrations varied with time, the average and 90th centile concentrations have remained relatively constant. Examination of frequency distributions for nonylphenol (NP) concentrations indicated that 99% of the levels in fresh surface waters are below the U.S. Environmental Protection Agency's Aquatic Life Ambient Chronic Water Quality Criteria for NP (6.6 μg/L). A conservative evaluation of aggregated NPEO/NPEM concentrations suggested that 97% of the samples contained aggregate NP equivalent concentrations that are also below 6.6 μg/L. These results suggest that on a nationwide basis, the likelihood of surface water concentrations exceeding the chronic USEPA Water Quality Criterion for NP is low. [ABSTRACT FROM AUTHOR]

Nonylphenol ethoxylates (NPE) are widely used surfactant compounds with many domestic and industrial applications. Due to the nature of their use in down-the-drain applications, spent NPE are discharged to septic systems or to wastewater treatment plants. Biodegradation of parent material during treatment is often incomplete, leading to release of NPE and their degradation intermediates into the environment. Considerable aquatic toxicity research has occurred on NPE and particularly on nonylphenol (NP). Available data were subjected to a quality review and all studies of acceptable quality were used in a weight of evidence hazard assessment. Data for NP were further analyzed using a Species Sensitivities Distribution (SSD) approach. About 90 chronic values are available (ChVs, geometric mean of the no-observed effect concentration and lowest-observed effect concentration for each endpoint reported), which may be reduced to average ChVs for each tested species. Higher mole NPE (NPE≥9) had ChVs ranging from 900 to 14,100μg/L, ChVs for the low mole nonylphenol ether carboxylate (NPEC1) ranged from 3200 to 12,000μg/L, ChVs for lower mole NPE (NPE1,2) ranged from 11 to 500μg/L, and ChVs for NP ranged from 5 to 3500μg/L. Using the SSD analysis for NP with higher quality study results, the 10th percentile chronic effect value is 5.7μg/L, which supports the draft USEPA criteria on NP of 5.9μg/L. [ABSTRACT FROM AUTHOR]

Bisphenol A (BPA; 4,4-isopropylidene diphenol) is a chemical intermediate used primarily in the production of epoxy resins and polycarbonate products. BPA has been identified in surface waters and, hence, has been the subject of considerable research into its potential effects on aquatic organisms. Available literature on the aquatic toxicity of BPA was reviewed for quality against European Union TGD and Organization of Economic Cooperation and Development GLP principles. From this review, studies of suitable quality covering numerous ecologically relevant endpoints were identified to evaluate the survival, growth, and reproductive success of aquatic organisms exposed to BPA. Those studies yielded approximately 70 no observed effect concentrations (ranging from 16 to 3640 µg/L) and lowest observed effect concentrations (160 to 11,000 µg/L) that were considered in this weight of evidence assessment. Across all data, adverse effects on survival, growth, and reproduction occurred only at concentrations of 160 µg/L and above. Secondary biochemical (e.g., vitellogenin induction) and morphological (e.g., gonad histology) data provide insight into mechanisms of action, but do not correlate with apical endpoints related to survival, growth, and reproduction. Comparing the weight of the evidence of the aquatic toxicity data that showed chronic effects at 160 µg/L and higher with typical surface water concentrations in the range of 0.001 to 0.10 µg/ L, BPA is unlikely to cause adverse effects on aquatic populations or ecosystems. [ABSTRACT FROM AUTHOR]