Risk Assessment Of Environmental Hazards Research Articles

Identifying organic micropollutants' transformation products from the soil dissipation experiment by non-targeted high-resolution mass spectrometry approach: Can we gain more than transformation product identity?

Risk assessment of environmental hazards originating from xenobiotics extensively used worldwide (e.g., pharmaceuticals, bisphenols, or preservatives) requires a combined study of their effects, mobility, dissipation mechanisms, and subsequent transformation product identification and evaluation. We have developed an efficient accelerated solvent extraction method for a broad range of micropollutants of variable physical-chemical properties in soils to enable more accurate hazard characterisation. Micropollutant recoveries from freeze-dried soils were 60–120%, with the exception of atorvastatin, fexofenadine, and telmisartan, which had reduced recoveries (40–66%). The observed matrix effect ranged from −26% to 17% and was corrected by the matrix matching standard for quantitative analysis. The method allows sensitive and reliable determination of a wide range of analytes in soil samples and, consequently, qualitative analysis of transformation products (TP) with variable physicochemical properties. We identified TPs of five compounds (venlafaxine, telmisartan, valsartan, atorvastatin, and sertraline) by applying suspect and non-targeted data analyses. To our knowledge, the transformation product of atorvastatin was reported for the first time. All others were found in soil or other matrices. Valsartan (formed valsartan acid) and atorvastatin (transformed probably by oxidative decarboxylation of beta, delta dihydroxy heptanoic acid chain to propionic acid) were modified to a relatively large extent. All other compounds identified were only hydroxylated (sertraline and telmisartan) or demethylated (venlafaxine). We estimated the stability and presence of the identified TPs based on the constructed time trends and the ratio between TP formation and degradation rates. We demonstrated how valuable a non-targeted approach can be for complex evaluation of the fate and effect of soil pollutants.

Quantitative Risk Assessment of Environmental Hazards Generated by a Tailings Embankment: case study Cabeço do Pião, Portugal

The Panasqueira mine is a world-class tungsten mine and probably one of the most important in Europe, having been continuously in operation since 1898. Between 1927 and 1996, the ore was fully or partially processed in a processing plant located on the left bank of the Zêzere River. The tailings were stored along the bank, in an extension of about 1.5 km. The fine particles, locally known as ‘sludge’, were stored in a self-constructed embankment located on a steep hillside. The current average slope is about 36°. The sludge has high concentrations of some heavy metals (Cu, Zn, W and Cd) but has a particularly high concentration in arsenic (about 15%). This tailings storage was not included in the National Plan for Rehabilitation of Abandoned Mines, despite presenting a high environmental risk. A quantitative environmental risk assessment characterises this situation, considering two possible alternatives: the current state with continuous release of contaminants or, alternatively, the situation that would arise from an eventual collapse of the storage embankment. In the first situation, we used a classical methodology of risk assessment to estimate the concentrations of arsenic in the affected compartments using a conservative exposure scenario and inferring the doses to which the local population is subjected. These doses are compared with reference acceptable values. In the second situation, the creation of a dispersed source of contamination encompasses a much higher dispersion area, a larger population and more expensive rehabilitation costs.

A review of methods used for hazard identification and risk assessment of environmental hazards

BackgroundApproximately one quarter of all deaths globally are attributed to living or working in an unhealthy environment, with household and ambient air pollution, along with exposures to ultraviolet radiation and chemicals amongst the leading causes. At present there are no international standards for assessing the risks of these environmental hazards. The use of heterogeneous methods to identify health risks from environmental hazards may reduce the level of confidence the public has in the conclusions that are made. ObjectivesTo describe and compare the processes and methods used by national and international organisations that conduct hazard identification and/or risk assessment (HI/RA) of environmental hazards and to identify knowledge gaps to inform the development of future methods. MethodsWe searched the websites of 19 organisations (ten national, five international and four World Health Organization (WHO) units) and extracted data from all relevant, publicly available resources which described the processes and methods used in HI/RA of environmental hazards. We contacted each organisation for any additional information. ResultsFive organisations were excluded from further analysis: three made recommendations but did not conduct HI/RA; one used heterogenous methods across their reviews for HI; and one WHO unit did not have any published guidelines. Of the 14 organisations analysed, five (36%) describe the process for establishing the questions to be answered in the assessments. Only one (7%) organisation uses systematic review methods, although five (36%) state that they use such methods. Ten (71%) assess the scientific quality of the included studies, however only three (21%) use explicit criteria. Only three (21%) organisations assess the quality of the body of evidence using explicit criteria. Four (29%) organisations describe the process for making the final HI conclusions and three (38%) the final RA conclusions. Eight (57%) have a conflict of interest policy and seven (50%) organisations describe a process for managing them. The US Office of Health Assessment and Translation and the World Health Organisation meet the most criteria for describing their processes and methods. ConclusionsThe processes and methods used by organisations conducting HI/RA of environmental hazards are inconsistent. There is a need for empirically based tools and methods to be adopted for the evaluation and synthesis of evidence, and the formulation of conclusions across all organisations that conduct HI or RA. These tools and methods will lead to increased transparency, comparability and validity of the assessments.

Risk Assessment and Epidemiologic Evidence: Kundi Responds

I appreciate Goldstein’s remarks about the role of epidemiology in risk assessment of environmental hazards and the opportunity to clarify my standpoint. With reference to the International Agency for Research on Cancer’s classification scheme of agents for their carcinogenicity in humans and other schemes such as that of the U.S. Environmental Protection Agency (EPA), Pitot and Dragan (2001) stated in Casarett and Doull’s Toxicology: In spite of the limitations of these classifications, an agent cannot be proven to be carcinogenic for the human unless substantial epidemiologic evidence supporting such a claim is available. Although this statement refers to carcinoma and not to the broader class of chronic diseases, it seems to be very close to my statement (Kundi 2006) that Goldstein criticizes. However, Goldstein particularly emphasizes that I may have meant that “there must be epidemiologic evidence for a chemical to achieve the level of a known or proven cause of a hazard to human health.” The reader may have noticed that I never used the term “proven” (Kundi 2006), and I deliberately did not. In my opinion we cannot reach the level of a proven cause. Our knowledge is always incomplete; although we may be quite sure about a factor causing a disease, it may turn out to be actually unrelated. Using toxicologic evidence, we may conjecture that an agent has a potential to cause human chronic disease, but we need further evidence—in most cases epidemiologic evidence—to establish a causal relationship between the agent and a chronic disease in humans. (I make a conceptual difference between “establishing” and “proving,” the latter defined as “establishing truth,” which can only be done for analytical statements.) My statement that Goldstein criticizes was misleading insofar as it seems to indicate that we have to start from epidemiologic evidence to ascribe an agent a hazardous potential for human health. In many cases first information on a potential hazard will stem from routine toxicologic testing. The last paragraphs of my commentary (Kundi 2006) were intended to give an outlook to future developments that may provide answers to the question of causation of chronic diseases in a more rapid fashion. From this context it should be clear that risk assessment was addressed with respect to the causal role of an agent. Therefore, a slight modification of the statement above is appropriate: An agent cannot be established to cause a chronic human disease unless supporting epidemiologic evidence is available. Among other improvements, comprehensive utilization of modern molecular biological methods integrated into epidemiologic designs may provide such evidence at an early stage of the disease.

Environmental hazard analysis and effective remediation of highway seepage

Risk assessment and minimisation of environmental hazards are critical issues to consider in the geotechnical engineering projects. A case of highway pavement seepage induced by groundwater, at a locality along the section of Hua-Qing Highway of Guangdong Province, China, is presented for environmental hazard analysis and effective remediation. The environmental hazard analyses were based on in situ hydrogeologic investigation, rock–soil testing and integrated environmental understanding. The analyses indicate that the highway seepage was caused by elevation of groundwater hydraulic pressure in low permeable strata near the highway pavement, which was controlled by landform, hydrology, weather and road structure. The risk source of groundwater ‘flooding’ was the groundwater and surface water in the ring-like valley around Fenshui Village. A blind-ditch system for effective remediation of the pavement seepage hazard was proposed and successfully implemented by declining groundwater table near the highway based on the comprehensive assessment of various conditions. This geotechnical accident shows that the role of groundwater is an essential factor to consider in the geotechnical and environmental engineering studies and multidisciplinary effort for risk assessment of environmental hazards is important under current global climate change condition.

ヒト由来細胞培養系を用いた水環境試料中の有機塩素化合物の毒性評価

As part of validation processes of in vitro toxicity assays for the risk assessment of environmental hazards, we applied an in vitro toxicity test using two human cell lines, neuroblastoma NB-1 cells and glioblastoma U-87 MG cells, to the assessment of organochlorine compounds detected in the water environment. The in vitro toxicity assay using NB-1 cells was calibrated by testing reference chemicals proposed by MEIC (Multicenter Evaluation of In Vitro Cytotoxicity), an international program for the validation of in vitro cytotoxicity assays.Beforehand, an assay using cells in frozen stock without subcultivation was examined by comparing IC50 values with the ordinary assay using subcultured cells. IC50 values for MEIC reference chemicals from the former assay showed good correlation with those from the latter assay, suggesting that the assay using cells in frozen stock can he used at least for the assessment of basal cytotoxicity.IC50 values for ten organochlorine compounds frequently detected in the sediment samples from contaminated rivers, p-chloroaniline, 3,4-dichloroaniline, p-dichlorohenzene, o-dichlorobenzene, Tris (2-chloroethyl)-phosphate, 2,5-dichlorophenol, 2,5-dichloroanisol, Triclosan and Triclocarban, were obtained with the in vitro assays and compared with their LD50 values in rats. No significant correlation, however, was seen between the IC50 and LD50 values, indicating that further improvement of in vitro toxicity assays is necessary for the application to the risk assessment of environmental hazards.

Paustenbach DJ (ed): The Risk Assessment of Environmental Hazards—A Textbook of Case Studies. New York, NY, Wiley, 1989, 1155 pages.

Paustenbach DJ (ed): The Risk Assessment of Environmental Hazards—A Textbook of Case Studies. New York, NY, Wiley, 1989, 1155 pages.

Paustenbach DJ (ed): The Risk Assessment of Environmental Hazards—A Textbook of Case Studies. New York, NY, Wiley, 1989, 1155 pages.

Paustenbach DJ (ed): The Risk Assessment of Environmental Hazards—A Textbook of Case Studies. New York, NY, Wiley, 1989, 1155 pages.

The Risk Assessment of Environmental Hazards, ed. D. J. Paustenbach [Review

The Risk Assessment of Environmental Hazards, ed. D. J. Paustenbach [Review

Quantitative risk assessment of environmental hazards.

Quantitative risk assessment may never become a rigorous scientific discipline because of the inherent difficulties in working with highly uncertain and often controversial data and methods, and because the predictions of risk assessment may not be subject to validation in their most important areas of application. However, the potential benefits of having quantitative estimates of risk may make quantitative risk assessment a valuable adjunct to traditional methods for making individual and social decisions about health hazards in the home, workplace, and general environment. Risk assessment, which is the process of estimating risks to populations exposed to hazardous agents or activities, must be distinguished from risk management, which is the process of forming and implementing a strategy for accepting or abating the risks. To the extent possible, these two processes should be kept separate. Quantitative risk assessment is in principle capable of estimating individual or lifetime excesses of specific health effects from exposures to a specified hazard. These excesses may be estimated on an absolute basis or expressed as a relative risk in comparison with the baseline risk that would exist without exposure. An individual risk is usually expressed in terms of the probability of developing the health effect in some time period following a specified exposure, whereas a population risk is the overall number of effects expected in a defined population with a defined distribution of exposure levels and patterns. The variation of risk with time after exposure may imply a constant absolute risk, a constant relative risk, or some other dependence on time, usually after a minimal latent period has elapsed. Risk estimates can rarely be made directly from observed human data, and models for extrapolating or projecting risk estimates from the conditions of observation to the actual conditions of exposure must be used. Dose-response relationships are used for extrapolating from high laboratory or occupational exposures to low exposures encountered more frequently in human populations. Thresholds of dose or nonlinear dose-response relationships may be related to nonlinear pharmacokinetics prior to the ultimate exposure of the critical organ to the proximate carcinogen or other hazardous agent. Time-response models estimate risks for periods after exposure longer than have been observed in epidemiologic studies. Extrapolations from experiments with laboratory animals to humans are made difficult because of great differences in size, lifespan, physiology, and metabolism between human and animal.(ABSTRACT TRUNCATED AT 400 WORDS)

Quantitative Risk Assessment of Environmental Hazards

Quantitative Risk Assessment of Environmental Hazards

Risk Assessment of Environmental Hazards (SCOPE Report No. 8), by Robert W. Kates. John Wiley, Chichester–New York–Brisbane–Toronto: xvii + 112 pp., figs & tables, 22.5 × 15 × 1 cm, paperbound, £4.95, 1978.

Risk Assessment of Environmental Hazards (SCOPE Report No. 8), by Robert W. Kates. John Wiley, Chichester–New York–Brisbane–Toronto: xvii + 112 pp., figs & tables, 22.5 × 15 × 1 cm, paperbound, £4.95, 1978. - Volume 6 Issue 2