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PubMedDate not supplied

The rationale for a ban on detergent phosphate in the Great Lakes Basin.

Immediate reduction of phosphorus loadings to the Great Lakes is essential to slow accelerated eutrophication. The Great Lakes National Program Office of the US Environmental Protection Agency now advocates adoption of bans on detergent phosphates as the most practical and feasible means of immediately reducing the phosphorus loadings to the Great Lakes. This change in policy from previous reliance on removal by sewage treatment has been adopted for the following reasons: (1) Bans on phosphates will reduce capital and operating costs of treatment and, were adopted, have met with consumer acceptance. (2) In practice, treatment plants have not met design expectations for phosphate removal. (3) Neither nitrilotriacetic acid nor other substitutes for phosphates have proved to be a public health problem. (4) Reduction of phosphorus loadings to treatment plants avoids increasing levels of chlorides and total dissolved solids in effluents. (5) Water quality has improved in small lakes with phosphorus reduction. In summary, detergent phosphate bans alone will not reduce phosphorus loadings to the Great Lakes sufficiently for the long term but the Environmental Protection Agency has concluded that such action is necessary in addition to continued efforts to control non-point sources.

Detergents↗
PubMed2000

Air pollution and health.

OBJECTIVE: To review the effects of air pollution on health, with special reference to data obtained locally in Hong Kong. DATA SOURCES: Medline literature search (1960-1999), websites of the World Health Organization and Environmental Protection Department, Hong Kong, and a report from the Sub-Working Group on the Review of Hong Kong's Air Quality Objectives, 1999. STUDY SELECTION: Key words for the literature search were 'air pollution' and 'health'. DATA EXTRACTION: The author reviewed relevant information and data. DATA SYNTHESIS: In many parts of the world and in Hong Kong, air pollution is associated with increased mortality and morbidity rates, as reflected by increased hospital admissions and doctor visits, not only for respiratory illnesses but also for cardiovascular illnesses. Some studies have found that air pollution is also associated with an increase in respiratory symptoms in lower lung function in children. In Hong Kong, air pollution is mostly because of traffic emissions. During the past decade, the annual mean levels of respirable suspended particulates and oxides of nitrogen and ozone have increased and exceeded the air quality objectives set by the Environmental Protection Department of Hong Kong. CONCLUSION: The medical profession should be concerned about the health effects of air pollution and should call for action to reduce the current levels of air pollution to an acceptable level.

Air Pollutants↗
PubMed2006

Effect of humic substance on thermal treatment of chromium(VI)-containing latosol soil.

Latosol soils contaminated with chromium(VI) [Cr(VI)], which is hazardous, can be recycled as raw materials for porcelain and construction sectors if a proper thermal stabilization process is implemented. This study investigates how thermal treatment affects Cr behavior during the sintering of latosol and deorganic latosol samples; both samples are artificially contaminated with CrO3. Approaches including X-ray absorption spectroscopy, scanning electron microscopy, N2-based Brunauer Emmett Teller surface analyzer, thermogravimetric analyzer/differential scanning calorimeter, and the toxicity characteristic leaching procedure promulgated by Taiwan Environmental Protection Administration are used in this study. After drying the Cr(VI)-contaminated latosol (i.e., containing 37,120 mg of Cr/kg sample) at 105 degrees C, approximately 80% of the doped CrO3 is chemically reduced to Cr(OH)3 by a humic substance naturally existing in the soil. In contrast, in the organics-free CrO3-contaminated latosol dried at 105 degrees C, only 9% of the doped CrO3 is reduced to Cr(OH)3. Heating the samples at 500 and 1100 degrees C transforms hazardous Cr(VI) into Cr(III) that is negligibly toxic; Cr2O3, which is insoluble, is detected as the most abundant Cr species. Moreover, formation of Cr2SiOs, which is suggested to relate to low Cr leaching, is only detected in the sample heated at 1100 degrees C. Surface morphology, surface area, and thermogravimetric analyzer/differential scanning calorimeter results demonstrate that thermal treatment at 1100 degrees C can incur considerable soil sintering/ melting if the humic substance in the soil has been heated off previously. Finally, Cr concentrations in the toxicity characteristic leaching procedure leachates collected from the samples thermally treated at 1100 degrees C for 4 hr are < or =0.21 mg of Cr L(-1) that are much less than the Taiwan Environmental Protection Administration regulatory limit (<5 mg of Cr L(-1)); consequently, these two samples are nonhazardous, and they have the potential for resource recycling. Conversely, Cr concentrations in the leachates from all 500 degrees C and 105 degrees C samples are in the 25.6-1279 mg L(-1) range.

Calorimetry, Differential Scanning↗
PubMed1992

Protection from environmental tobacco smoke in California. The case for a smoke-free workplace.

OBJECTIVE: To determine the extent of exposure of nonsmoking indoor workers to environmental tobacco smoke (ETS) according to type of work-site smoking policy, work area, workplace size, and demographic characteristics. DESIGN AND PARTICIPANTS: Participants included 7162 adult, nonsmoking, indoor workers who were interviewed as part of the 1990 California Tobacco Survey. Respondents were asked whether anyone had smoked in their work area within the past 2 weeks. RESULTS: An estimated 2.2 million California nonsmokers were exposed to tobacco smoke at indoor work sites in 1990. Nonsmoker exposure to ETS was 9.3% for those working in a smoke-free worksite, 23.2% for those working where there was only a work-area restriction, 46.7% for those working where there was a policy that did not include the work area, and 51.4% for those working where there was no work-site smoking policy. After adjustment for type of work area (eg, office, open area), workplace size, and demographic factors, it was determined that nonsmokers working where there was only a work-area ban were 2.8 times more likely to be exposed to ETS than those working in a smoke-free work site. In workplaces with no policy or a policy not covering the work area, nonsmokers were over eight times more likely to be exposed to ETS than those who worked in a smoke-free work site. Nonsmokers who were 18 to 24 years of age, male, or Hispanic, and those with less than a high school education had more exposure to ETS. CONCLUSION: These results indicate that adequate protection of nonsmokers from ETS exposure requires a smoke-free work site.

Adolescent↗
PubMed2004

Effects of pyrethroids on voltage-sensitive calcium channels: a critical evaluation of strengths, weaknesses, data needs, and relationship to assessment of cumulative neurotoxicity.

The Food Quality Protection Act of 1996 requires that the U.S. Environmental Protection Agency conduct cumulative risk assessments for classes of pesticides that have a common mode or mechanism of action. For the pyrethroid insecticides, disruption of voltage-sensitive sodium channel function is generally accepted as the mechanism underlying acute neurotoxicity. However, data exist which suggest that voltage-sensitive calcium (Ca(2+)) channels (VSCC) may also be important targets of pyrethroid action. VSCC are important to neuronal function during development and for neurotransmitter release, gene expression, and electrical excitability in the nervous system. Disruption of these and other processes mediated by VSCC can result in neurotoxicity. If effects on VSCC are demonstrated to contribute to pyrethroid neurotoxicity, then such effects will have to be considered when making decisions regarding cumulative risk of exposure to this class of compounds. This document provides a critical review of the data related to the hypothesis that VSCC are important targets of pyrethroid effects. Data supporting effects of pyrethroids on VSCC have been generated by several different laboratories using different techniques and biological preparations. Thus, the many reports of effects on VSCC provide evidence that pyrethroids may interact with VSCC. However, evidence to support a role of VSCC in pyrethroid neurotoxicity is based entirely on in vitro observations, and numerous limitations exist in these data, including: (1) lack of defined concentration-response relationships, with some effects observed only at relatively high concentrations, (2) the use of indirect measures of VSCC function, (3) data from nonmammalian species, (4) data from studies that have not been peer-reviewed, (5) the need for replication of some effects, and (6) inconsistent or contradictory results from different laboratories/preparations. Thus, at the present time, it is premature to conclude that effects on VSCC play an important role in the acute neurotoxicity of pyrethroid insecticides in mammals. To demonstrate that VSCC are important targets of pyrethroid neurotoxicity in mammals, in vivo studies supporting a role for pyrethroid effects on VSCC are needed. Additional support could be provided by demonstration of direct effects of pyrethroid compounds on mammalian neuronal VSCC in vitro, including demonstration that concentration-response relationships are similar, or greater, in sensitivity to effects of pyrethroids on voltage-sensitive sodium channels. If such effects were to be demonstrated, the rationale for considering VSCC as targets of pyrethroid compounds when assessing cumulative risk would be strengthened. However, at the present time, the data available neither support nor refute conclusively the hypothesis that effects on VSCC are important to the acute neurotoxicity of pyrethroids.

Animals↗
PubMed2003

Development and evaluation of a Macroinvertebrate Biotic Integrity Index (MBII) for regionally assessing Mid-Atlantic Highlands Streams.

The Macroinvertebrate Biotic Integrity Index (MBII) was developed from data collected at 574 wadeable stream reaches in the Mid-Atlantic Highlands region (MAHR) by the U.S. Environmental Protection Agency's (USEPA) Environmental Monitoring and Assessment Program (EMAP). Over 100 candidate metrics were evaluated for range, precision, responsiveness to various disturbances, relationship to catchment area, and redundancy. Seven metrics were selected, representing taxa richness (Ephemeroptera richness, Plecoptera richness, Trichoptera richness), assemblage composition (percent non-insect individuals, percent 5 dominant taxa), pollution tolerance [Macroinvertebrate Tolerance Index (MTI)], and one functional feeding group (collector-filterer richness). We scored metrics and summed them, then ranked the resulting index through use of independently evaluated reference stream reaches. Although sites were classified into lowland and upland ecoregional groups, we did not need to develop separate scoring criteria for each ecoregional group. We were able to use the same metrics for pool and riffle composite samples, but we had to score them differently. Using the EMAP probability design, we inferred the results, with known confidence bounds, to the 167,797 kilometers of wadeable streams in the Mid-Atlantic Highlands. We classified 17% of the target stream length in the MAHR as good, 57% as fair, and 26% as poor. Pool-dominated reaches were relatively rare in the MAHR, and the usefulness of the MBII was more difficult to assess in these reaches. The process used for developing the MBII is widely applicable and resulted in an index effective in evaluating region-wide conditions and distinguishing good and impaired reaches among both upland and lowland streams dominated by riffle habitat.

Animals↗
PubMed1995

International Commission for Protection Against Environmental Mutagens and Carcinogens. Genetic risk extrapolation from animal data to human disease. A Taskgroup Report. No. 00105.

This report describes a model for producing quantitative genetic risk assessments for human populations. The model is patterned after current methods used in cancer risk analysis. The risk to humans is expressed as the number of additional dominant genetic diseases added to the existing genetic burden, in the offspring of the exposed individuals.

Animals↗
PubMed1995

International Commission for Protection against Environmental Mutagens and Carcinogens. An evaluation of the genetic toxicity of paracetamol.

During the last years, several reports have indicated genotoxic effects of paracetamol, a widely used non-prescription analgesic and antipyretic drug. Thus, a careful evaluation of a possible genotoxic effect related to paracetamol use is warranted. Studies in vitro and in vivo indicate that the reactive metabolite of paracetamol can bind irreversibly to DNA and cause DNA strand breaks. Paracetamol inhibits both replicative DNA synthesis and DNA repair synthesis in vitro and in experimental animals. Paracetamol does not cause gene mutations, either in bacteria or in mammalian cells. On the other hand, a co-mutagenic effect of paracetamol has been reported. Furthermore, paracetamol increases the frequency of chromosomal damage in mammalian cell lines, isolated human lymphocytes and experimental animals. Two independent studies have shown an increase in chromosomal damage in lymphocytes of human volunteers after intake of therapeutic doses of paracetamol, whereas a third study was negative. Paracetamol-induced chromosomal damage appears to be caused by an inhibition of ribonucleotide reductase. This indicates that a threshold level for the paracetamol-induced chromosomal damage may exist. Genotoxic effects of paracetamol have, however, been demonstrated both in vitro and in vivo at or near therapeutic concentrations. The data indicate that the use of paracetamol may contribute to an increase in the total burden of genotoxic damage in man. Thus, there may be a need to evaluate the therapeutic benefit of paracetamol, taking into consideration not only its potential to induce acute and chronic organ damage, but also genotoxic effects.

Acetaminophen↗
PubMed1994

International Commission for Protection Against Environmental Mutagens and Carcinogens. Mutagenicity and carcinogenicity of topoisomerase-interactive agents.

Drugs that interact with DNA topoisomerases I and II hold great promise for the treatment of cancer, however, like many other anti-cancer agents, they are a double-edged sword and may themselves cause mutation and cancer. In vitro studies show that clinically effective agents, such as etoposide, doxorubicin and others, stabilize a ternary complex where topoisomerase II is covalently linked to DNA. This complex represents an intermediate in the topoisomerase-II catalyzed DNA supercoil relaxation reaction. Camptothecin and its analogues stabilize a similar ternary complex, in vitro, consisting of topoisomerase I covalently linked to DNA at single-strand breaks. Short-term tests of genotoxicity confirm that topoisomerase-interactive agents are mutagenic and suggest common mechanisms by which they induce mutation and selectively kill tumor cells. These agents induce sister-chromatid exchange, chromosomal aberrations and mutations in specific mammalian genes. Their propensity to induce small colonies in the L5178/TK+/(-)-3.7.2C assay implies that topoisomerase-interactive agents induce large DNA rearrangements and deletions. These may result from topoisomerase-subunit exchange at drug-stabilized ternary complexes or from attempts by the cell to bypass the replication block caused by stabilized ternary complexes. Studies in bacterial mutation assays suggest that topoisomerase-interactive agents may also induce mutations, albeit at a lower rate, through simple DNA intercalation or via generation of oxygen free radicals. Second malignancies observed in patients previously treated with topoisomerase II interactive agents suggest these may be an important clinical consequence of their capacity to induce mutation. In particular, a unique form of acute myelogenous leukemia is observed at strikingly high frequencies after treatment with relatively high doses of the epipodophyllotoxins etoposide and teniposide. This form of AML has been reported after the uses of other classes of topoisomerase-interactive agents as well. Cancer induction is therefore a toxic consequence predicted by short-term tests of genotoxicity and should be weighed against the potential therapeutic benefits of topoisomerase-interactive agents.

Animals↗
PubMed1994

International Commission for Protection Against Environmental Mutagens and Carcinogens. Two million rodent carcinogens? The role of SAR and QSAR in their detection.

The accurate prediction of chemical carcinogenicity can only be achieved by a balanced consideration of the following factors: the chemistry and metabolism of the test agent, the interaction between toxicity and genetic toxicity, the possibility of non-genotoxic events that trigger subsequent non-targeted mutagenesis, the difference between activities observed in vitro and in vivo, and the possible inadequacy and/or partiality of all datasets and observations. Extrapolation of activities within a series of congeners is usually possible, but predictions across different chemical classes/mechanisms of carcinogenicity are difficult. Artificial intelligence systems can be used to predict one or more of the above parameters given adequate learning sets, but the hope for a single, coherent and self-contained method of predicting all instances of carcinogenicity is unreal. The future of carcinogen/mutagen prediction lies with data-rich artificial intelligence systems based on known mechanistic principles used selectively within the context of chemical and biological human insight. The major current obstacle to progress is the assumption that mutagenicity and carcinogenicity are unitary phenomena that can be learned and predicted by artificial intelligence systems operating in isolation.

Alkylating Agents↗
PubMed1994

International Commission for Protection Against Environmental Mutagens and Carcinogens. The subtlety of alkylating agents in reactions with biological macromolecules.

Genotoxic agents known to modify DNA by alkylation reactions (alkylating agents, AAs), either directly or after metabolic conversion to ultimately reactive intermediates, by no means represent a homogeneous class. For instance, their effectiveness for genotoxic damage, when expressed as the number of events (e.g., mutations) per unit exposure dose, varies over a more than 1-million-fold range in dose. Despite the multiplicity of chemical and biological processes involved between DNA adduct formation and expression of genotoxic damage, the principal aims of studies on structure-activity relationships (SARs) are to (a) dissect the multi-step process of genetic damage formation into its most essential components, (b) use SARs for making predictions and, at a later step (c) as a basis for regulatory measures. The analytical tools available for such a comprehensive analysis in eukaryotic systems include determination of multiple genetic endpoints: molecular mutation spectra, relative clastogenicity (clastogenic events in relation to forward mutation induction) and the quantitative measure of enhanced mutagenicity in repair-deficient conditions. The genetic activity profiles obtained in this way can then be compared with fundamental physico-chemical properties of the AAs under consideration (such as Swain-Scott's s value, a useful indicator of the selectivity of an AA in its reactions with nucleophiles of distinct nucleophilic strength n in DNA, RNA and proteins), their functionality (monofunctional versus cross-linking) and their tumorigenic potency (TD50s compared with measures of initial DNA interaction, i.e., O6-/N7-alkylguanine ratios, s values or the covalent binding index determined in the liver in vivo). The combination of these different methods revealed that carcinogenic potencies of AAs in rodents vary over a 10,000-fold range in dose, with the extremes having the following characteristics: (i) Chemicals of a relatively "high carcinogenic potency", as indicated by a low TD50 in rodents, either have low nucleophilic selectivity (and therefore mainly act through O-alkylation in DNA) or are capable of cross-linking DNA. The monofunctional members of this group, typified by N-ethyl-N-nitrosourea, are active in both spermatogonia and post-spermatogonial stages in the mouse and in Drosophila. Cross-linking agents also have a low TD50 value in rodents but are expected generally not to display genetic action in premeiotic stages (exceptions mitomycin C and chlorambucil). (ii) A relatively low carcinogenic potential is associated with AAs of high Swain-Scott s values, typified by trimethyl phosphate, epichlorohydrin or methyl methanesulphonate.(ABSTRACT TRUNCATED AT 400 WORDS)

Alkylating Agents↗
PubMed1994

International Commission for Protection Against Environmental Mutagens and Carcinogens. Approaches to SAR in carcinogenesis and mutagenesis. Prediction of carcinogenicity/mutagenicity using MULTI-CASE.

The assumptions and considerations underlying the use of structure-activity studies in the field of genotoxicity are discussed and reviewed. The MULTI-CASE program, recently introduced as a second generation CASE program is described and its special features highlighted. Some of the problems relevant to the use of structure-activity tools are also discussed. A list of these problems is as follows: Problems with non-congeneric data bases, Problems with expert systems, Problems with the size of the data bases, Problems with "structural alerts", Problems with QSAR, Problems with Metabolic transformations, and Problems with short-term assays.

Animals↗