Multicriteria decision analysis: a comprehensive decision approach for management of contaminated sediments.

Contaminated sediments and other sites present a difficult challenge for environmental decisionmakers. They are typically slow to recover or attenuate naturally, may involve multiple regulatory agencies and stakeholder groups, and engender multiple toxicological and ecotoxicological risks. While environmental decision-making strategies over the last several decades have evolved into increasingly more sophisticated, information-intensive, and complex approaches, there remains considerable dissatisfaction among business, industry, and the public with existing management strategies. Consequently, contaminated sediments and materials are the subject of intense technology development, such as beneficial reuse or in situ treatment. However, current decision analysis approaches, such as comparative risk assessment, benefit-cost analysis, and life cycle assessment, do not offer a comprehensive approach for incorporating the varied types of information and multiple stakeholder and public views that must typically be brought to bear when new technologies are under consideration. Alternatively, multicriteria decision analysis (MCDA) offers a scientifically sound decision framework for management of contaminated materials or sites where stakeholder participation is of crucial concern and criteria such as economics, environmental impacts, safety, and risk cannot be easily condensed into simple monetary expressions. This article brings together a multidisciplinary review of existing decision-making approaches at regulatory agencies in the United States and Europe and synthesizes state-of-the-art research in MCDA methods applicable to the assessment of contaminated sediment management technologies. Additionally, it tests an MCDA approach for coupling expert judgment and stakeholder values in a hypothetical contaminated sediments management case study wherein MCDA is used as a tool for testing stakeholder responses to and improving expert assessment of innovative contaminated sediments technologies.

Widespread arsenic contamination of soils in residential areas and public spaces: an emerging regulatory or medical crisis?

A critical review finds government agencies allow, permit, license, or ignore arsenic releases to surface soils. Release rates are controlled or evaluated using risk-based soil contaminant numerical limits employing standardized risk algorithms, chemical-specific and default input values. United States arsenic residential soil limits, approximately 0.4- approximately 40 ppm, generally correspond to a one-in-one-million to a one-in-ten-thousand incremental cancer risk range via ingestion of or direct contact with contaminated residential soils. Background arsenic surface soil levels often exceed applicable limits. Arsenic releases to surface soils (via, e.g., air emissions, waste recycling, soil amendments, direct pesticide application, and chromated copper arsenic (CCA)-treated wood) can result in greatly elevated arsenic levels, sometimes one to two orders of magnitude greater than applicable numerical limits. CCA-treated wood, a heavily used infrastructure material at residences and public spaces, can release sufficient arsenic to result in surface soil concentrations that exceed numerical limits by one or two orders of magnitude. Although significant exceedence of arsenic surface soil numerical limits would normally result in regulatory actions at industrial or hazardous waste sites, no such pattern is seen at residential and public spaces. Given the current risk assessment paradigm, measured or expected elevated surface soil arsenic levels at residential and public spaces suggest that a regulatory health crisis of sizeable magnitude is imminent. In contrast, available literature and a survey of government agencies conducted for this paper finds no verified cases of human morbidity or mortality resulting from exposure to elevated levels of arsenic in surface soils. This concomitance of an emerging regulatory health crisis in the absence of a medical crisis is arguably partly attributable to inadequate government and private party attention to the issue.

In vitro effects of N-nitrosoatrazine on chromosome breakage.

Exposing human lymphocyte cultures to concentrations of N-nitrosoatrazine (NNAT) as low as 0.0001 microgram/ml results in significant elevations in chromosome breakage as well as an increased mitotic index. In contrast, 1,000-10,000-fold greater concentrations of nitrates, nitrites, and/or atrazine was required to produce comparable chromosome damage and, in those cases where the mitotic index was affected, it was decreased. Simultaneous administration of nitrates or nitrites with atrazine caused less chromosome damage than low concentrations of NNAT without affecting the mitotic index, illustrating that metabolic conversion of contaminants with minimal genotoxicity can give rise to compounds such as NNAT which are even more genotoxic.

Cytogenetic studies of herbicide interactions in vitro and in vivo using atrazine and linuron.

The herbicides atrazine and linuron, found in Wisconsin's groundwater, were tested alone and in combination, both in vivo and in vitro, to determine their individual and combined genotoxic effects. Human lymphocytes exposed in vitro to either 1 microgram/ml linuron or 0.001 microgram/ml atrazine showed little chromosome damage, whereas significant chromosome damage was observed in lymphocytes simultaneously exposed to 0.5 microgram/ml linuron and 0.0005 microgram/ml atrazine, suggesting at least an additive model. In another experiment, mice were fed 20 micrograms/ml atrazine, 10 micrograms/ml linuron, or a combination of 10 micrograms/ml atrazine and 5 micrograms/ml linuron in their drinking water for 90 days, after which bone marrow cells and cultured splenocytes were examined for chromosomal damage. None of the treatment groups showed chromosome damage in bone marrow, whereas the cultured splenocytes demonstrated damage in all treatment groups. These experiments suggest that, prior to assessing the risk of a herbicide, it may be necessary to test it in combinations which mimic the mixtures which would occur under field conditions, such as in contaminated groundwater.

Cytogenetic effects of alachlor and/or atrazine in vivo and in vitro.

The purpose of this study was to assess the cytogenetic effects of two commonly used herbicides, alachlor and atrazine, which are often found together in groundwater. Chromosome damage was examined in bone marrow cells of mice drinking water containing 20 ppm alachlor and/or 20 ppm atrazine, with an immunosuppressive dose of cyclophosphamide used as a positive control. Chromosome damage was also quantified in human lymphocytes exposed in culture to 1.0, 0.1, or 0.01 microgram/ml alachlor and/or atrazine. The in vitro study demonstrated dose related cytogenetic damage not associated with mitotic inhibition or cell death, with damage due to the alachlor-atrazine combination suggesting an additive model. The in vivo study also suggested additive damage due to the alachloratrazine combination after 30 days of treatment, but, unexpectedly, demonstrated less cytogenetic damage and fewer cells with multiple aberrations after 90 days. Also, at 90 days, all treated mice had elevated mitotic indices compared to controls. The fact that the elevated mitotic index was associated with immune suppression in the cyclophosphamide group suggests that death of cells with accumulated chromosomal aberrations resulted in increased bone marrow proliferation, so a higher fraction of cells examined were newer with less damage. Since the alachlor-atrazine combination treated mice showed little systemic toxicity despite bone marrow mitotic indices similar to the cyclophosphamide treated animals, as well as a similar decrease in cytogenetic damage at 90 days compared to 30 days, cell death and replacement must also be involved but cannot completely explain the results.

Changes in T-lymphocyte distribution associated with ingestion of aldicarb-contaminated drinking water: a follow-up study.

The carbamate pesticide, aldicarb, is the most commonly found man-made groundwater contaminant in Wisconsin. A 1985 study linked ingestion of aldicarb-contaminated drinking water with altered T-cell distributions, specifically an increase in the mean number of CD8+ (T8) T cells. To further evaluate this finding, a follow-up study was done in 1987. Of the 50 Portage County, Wisconsin, women who participated in the first study, 45 participated in the follow-up: 18 formerly exposed and 27 formerly unexposed. In our follow-up study, only 5 women were found to be currently exposed to aldicarb. This group of 5 women, compared to 39 unexposed women who had peripheral blood specimens taken, had an increased percentage of lymphocytes and an increased number of CD2+ T cells, due to an increased number of total CD8+ T cells. Although the number of exposed persons was small, the increases in percentage lymphocytes and absolute numbers of CD2+ and CD8+ T cells were consistent with a dose-response relationship. No identified drinking water contaminant other than aldicarb could explain these findings. These results support earlier evidence linking aldicarb exposure and lymphocyte distribution changes. Although adverse clinical effects have not been documented, the widespread use of this chemical and consequent potential for widespread exposure indicate a clear need for further research on this issue.

Chronic exposure to aldicarb-contaminated groundwater and human immune function.

Aldicarb, a carbamate pesticide, has been a known groundwater contaminant in Wisconsin since 1981. To assess the effects of chronic ingestion of low-level aldicarb-contaminated groundwater (less than 61 ppb) on the immune function of humans, we identified 50 women, ages 18 to 70, with no known underlying reason for immunodysfunction. Twenty-three of these women (exposed group) consumed groundwater with detectable levels of aldicarb, and 27 (unexposed group) consumed water from a source with no detectable levels of aldicarb. Data were collected on each woman's health status, immune function, and fluid intake. Exposed women as compared with unexposed women showed an elevated stimulation assay response to the antigen Candida (P less than 0.02, t test). The exposed group had increased numbers of T8 cells (P less than 0.05, t test), an increased percentage of total lymphocytes as T8 cells (P less than 0.02, t test), and a decreased ratio of T4:T8 cells (P less than 0.02, t test). Our results suggest an association between consumption of aldicarb-contaminated groundwater and abnormalities in T-cell subsets in women with otherwise intact immune systems.