Identifying soil cleanup criteria for dioxins in urban residential soils: how have 20 years of research and risk assessment experience affected the analysis?

This article reviews the scientific evidence and methodologies that have been used to assess the risks posed by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and presents a probabilistic analysis for identifying virtually safe concentrations of TCDD toxicity equivalents (TEQ) in residential soils. Updated data distributions that consider state-of-the-science cancer and noncancer toxicity criteria, child soil ingestion and dermal uptake, bioavailability in soil, and residential exposure duration are incorporated. The probabilistic analysis shows that the most sensitive determinants of dose and risk are childhood soil ingestion, exposure duration, and the selected TCDD cancer potency factor. It also shows that the cancer risk at 1 per 100,000 predicted more conservative (lower) soil criteria values than did the noncancer hazard (e.g., developmental and reproductive effects). In this analysis, acceptable or tolerable soil dioxin concentrations (TCDD TEQ) ranged from 0.4 to 5.5 ppb at the 95th percentile for cancer potency factors from 9600 to 156,000 (mg/kg/d)(-1) with site-specific adjustments not included. Various possible soil guidelines based on cancer and noncancer risks are presented and discussed. In the main, the current toxicology, epidemiology, and exposure assessment data indicate that the historical 1 ppb TEQ soil guidance value remains a reasonable screening value for most residential sites. This analysis provides risk managers with a thorough and transparent methodology, as well as a comprehensive information base, for making informed decisions about selecting soil cleanup values for PCDD/Fs in urban residential settings.     

Identifying Soil Cleanup Criteria for Dioxins in Urban Residential Soils: How Have 20 Years of Research and Risk Assessment Experience Affected the Analysis?

This article reviews the scientific evidence and methodologies that have been used to assess the risks posed by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and presents a probabilistic analysis for identifying virtually safe concentrations of TCDD toxicity equivalents (TEQ) in residential soils. Updated data distributions that consider state-of-the-science cancer and noncancer toxicity criteria, child soil ingestion and dermal uptake, bioavailability in soil, and residential exposure duration are incorporated. The probabilistic analysis shows that the most sensitive determinants of dose and risk are childhood soil ingestion, exposure duration, and the selected TCDD cancer potency factor. It also shows that the cancer risk at 1 per 100,000 predicted more conservative (lower) soil criteria values than did the noncancer hazard (e.g., developmental and reproductive effects). In this analysis, acceptable or tolerable soil dioxin concentrations (TCDD TEQ) ranged from 0.4 to 5.5 ppb at the 95th percentile for cancer potency factors from 9600 to 156,000 (mg/kg/d)^?1 with site-specific adjustments not included. Various possible soil guidelines based on cancer and noncancer risks are presented and discussed. In the main, the current toxicology, epidemiology, and exposure assessment data indicate that the historical 1 ppb TEQ soil guidance value remains a reasonable screening value for most residential sites. This analysis provides risk managers with a thorough and transparent methodology, as well as a comprehensive information base, for making informed decisions about selecting soil cleanup values for PCDD/Fs in urban residential settings.     

A critical examination of assumptions used in risk assessments of dioxin contaminated soil

Environmental standards for 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin, TCDD) are currently being considered by regulatory agencies worldwide. Among these are limits for tap water, soil at industrial sites, residential soil, fish, ambient air, and fly ash. Thus far, in the United States, no standards have been promulgated but a few have been suggested. This paper critically evaluates several aspects of previously proposed approaches to setting limits for TCDD in residential soil and soil within industrial sites. Factors and assumptions which significantly affect the predicted degree of hazard associated with exposure to soil contaminated with low levels of dioxin are discussed. This paper shows how different, more justifiable assumptions than those used by the Centers for Disease Control (CDC) regarding the quantities of soil typically consumed by children, TCDD's nongenotoxicity, dermal exposure to soil, the concentration of airborne soil particles, dioxin's bioavailability in soil, and extrapolation of the dose response curve can profoundly affect the results of the risk assessment and, subsequently, the magnitude of the recommended limits. Two case studies which quantitatively illustrate the effect of these assumptions on the risk estimates are presented. Non-U.S. regulatory agencies have considered TCDD's nongenotoxicity in estimating that the virtually safe dose (VSD) or acceptable daily dose for dioxin is approximately 10 pg/kg/day (10,000 fg/kg/day). These approaches are compared and contrasted with the method used by the United States EPA whose risk estimates are higher and whose VSD is approximately 1,000-fold lower. Alternative approaches to interpreting the cancer data indicate that a VSD of 130 pg/kg/day is more scientifically justified than risks estimated using standard approaches. This assessment indicates that a soil concentration of TCDD considerably in excess of 1 ppb should be acceptable for residential and nonresidential areas.     

A proposed approach to regulating contaminated soil: identify safe concentrations for seven of the most frequently encountered exposure scenarios.

Since 1980, more than 10,000 sites in the United States have been shown to contain soil which has elevated concentrations of various xenobiotics. Since that time, guidelines for deciding whether the level of contamination is worthy of concern have been proposed or promulgated by dozens of local, state, and federal regulatory agencies. Unfortunately, there has been little consistency in the guidelines suggested for each soil contaminant. For example, (a) the basis or rationale for some of the cleanup levels is unclear, (b) approaches to setting cleanup levels vary between states and agencies, (c) cleanup objectives often vary among agencies within the same state, and (d) the cleanup levels are usually set in a scientifically haphazard manner. This paper proposes that the most cost-effective and efficient way to quickly regulate contaminated soil is to establish "safe" concentrations for each chemical for the seven most common exposure scenarios. These exposure scenarios include (1) residential, (2) industrial, (3) agricultural, (4) recreational, (5) groundwater, (6) wildlife and aquatic species, and (7) runoff/erosion of particulates to waterways. The scientific approach and rationale for calculating the cleanup criteria are illustrated by evaluating dioxin and benzene, toluene, and xylene (BTX). The methods suggested here indicate that levels of dioxin of 25 and 50 ppb in residential and industrial soils, respectively, should be acceptable. The predominant concern for the agricultural and recreational scenarios is the runoff of particulates to waterways. For BTX, benzene will dictate the degree of cleanup and the primary hazard at most residential sites will be the inhalation of vapors. Benzene concentrations of 2.5, 14, and 250 ppm should be acceptable for residential, industrial, and recreational soils, respectively. Depending on the depth to groundwater and aquifer use, protection of groundwater may be the driving concern for establishing BTX cleanup levels and must be determined using site-specific factors.     

Assessment of the human health risks posed by exposure to chromium-contaminated soils

Millions of tons of chromite-ore processing residue have been used as fill in various locations in northern New Jersey and elsewhere in the United States. The primary toxicants in the residue are trivalent chromium [Cr(III)] and hexavalent chromium [Cr(VI)]. The hazard posed by Cr(III) is negligible due to its low acute and chronic toxicity. In contrast, Cr(VI) is a human carcinogen following inhalation of high concentrations. It can also cause allergic contact dermatitis. This evaluation addresses a residential site where the arithmetic mean (x) and geometric mean (gm) concentrations of Cr(III) in soil were 2879 and 1212 mg/kg (ppm). The mean and geometric mean concentrations of Cr(VI) were 180 and 4 mg/kg, respectively. The uptake (absorbed dose) of Cr(III) via soil ingestion, consumption of homegrown vegetables, and ingestion of inspired particles was determined. The uptake of Cr(VI) via dermal absorption from contact with surface soil and building wall surfaces, as well as inhalation, was also evaluated. The techniques used in this assessment are applicable for evaluating the human health risks posed by any residential site having contaminated soil. The potential for both sensitized and unsensitized persons to develop allergic contact dermatitis due to exposure to soil contaminated at these levels was found to be negligible. The estimated average daily dose (ADD) via ingestion and dermal absorption for the maximally exposed individual (MEI) was about 1500- and 40-fold below the EPA reference dose (RfD) for Cr(III) and Cr(VI), respectively. It was shown that for residential sites, the most important route of exposure to Cr(III) was incidental soil ingestion. Although not relevant to these sites specifically, if garden vegetables could be successfully grown in these soils, then they would probably be the predominant source of uptake of Cr(III). Since inhalation of Cr(VI)-contaminated dust (but not ingestion or dermal contact) poses a cancer hazard, the doses and associated risks were assessed. The estimated cancer risks for the MEI and most likely exposed individual (MLEI) were approximately 5 x 10(-9) and 2 x 10(-9), respectively. These levels of risk have always been considered well below those that warrant regulatory concern. For persons living on residential properties, the cancer risk due to inhaling suspended particles is likely to be less than 1 in 1,000,000 if Cr(VI) levels in soil are less than 180 mg/kg (ppm). Based on this analysis, the levels of Cr(III) and Cr(VI) at this and similar sites do not pose a health hazard following acute or chronic exposure.     

Human exposures from dioxin in soil--a meeting report

A 1984 risk assessment identified 1 part per billion (ppb) of dioxin in soil as a "level of concern" at Times Beach, Mo. The authors of the assessment had to rely on many assumptions in their analysis, but since that time, a number of investigators have obtained data that bear directly on estimating exposures from substances in soil. Partly because of the assumptions and partly because of the site-specific nature of their analysis, the authors of the Times Beach risk assessment cautioned against the adoption of 1 ppb as a delineator between acceptable and nonacceptable levels of contamination. Those cautions have been more frequently ignored than honored, and 1 ppb has become a de facto standard. In November 1989, the Center for Risk Management at Resources for the Future hosted 50 experts at a workshop that heard and discussed published and new research about exposure estimates and measures. The 1984 assessment identified soil ingestion by toddlers as the single most important source of exposure to dioxin in soil; it assumed that toddlers ingested 10 g soil daily. Research discussed at the workshop shows that the average child ingests about 0.04 g soil daily, but that 1 of 320 studied children ingested 5 g. These findings leave open the risk management decision about whether acceptable exposure levels should be established to protect the average child or the extreme child. Furthermore, the absence of children from commercial and industrial sites led to suggestions that higher concentrations of dioxin are acceptable in soil at such sites. Some workshop participants objected to those suggestions because of the difficulty of assuring that such sites would not revert to residential use in the future. Whether deed restrictions are sufficient to prevent such reversions was seen as an important research topic. Workshop participants repeatedly discussed the importance of site-specific data in estimating exposures: Measured half-lives of dioxin in different soils range from 18 mo to greater than 100 yr; bioavailability from various soils differs by at least 20-fold; and the amounts of soil ingested by grazing cattle can differ 20-fold depending on conditions. Workshop participants agreed upon some suggestions for research and generally favored the development of guidelines for exposure assessment that would allow consideration of site-specific information. Furthermore, they generally agreed that no single concentration should be taken as a level of concern. Instead, levels should be established that consider the planned uses of the sites.     

The health hazards posed by chromium-contaminated soils in residential and industrial areas: conclusions of an expert panel.

Between 1905 and 1971, over 2 million tons of residue from chromite ore processing was generated in Hudson County, New Jersey, of which substantial amounts were used as fill and tank diking. A panel of medical, toxicology, and risk assessment experts was convened in early 1990 to evaluate the potential health hazards posed by the resulting chromium contaminated soil. The Panel concluded that soils containing concentrations of 75 ppm hexavalent chromium [Cr(VI)] and 1000 ppm total chromium compounds (about 95% was trivalent chromium [Cr(III)]) did not pose a significant health hazard to nearby residents and workers. They also determined that exposure to chromium from Hudson County sites posed a negligible cancer hazard to residents. Using risk assessment methods, the Panel estimated that the plausible incremental cancer risk to individuals at residential sites would be substantially less than 1 in 1,000,000. The average measured levels of airborne Cr(VI) at typical industrial sites were more than 1000-fold lower than the current OSHA Permissible Exposure Limit (PEL). The maximum plausible increased cancer risk for an average worker at a dusty industrial site was estimated to be less than 1 in 100,000. The Panel also concluded that chromium-containing crystals, which have occasionally been found in Hudson County buildings, do not pose a significant hazard. However, they suggested that were the concentration to exceed 5000 ppm Cr(VI) in the crystals, site-specific health risk assessments would be conducted and remediation considered. The Panel evaluated the dermal hazard posed by chromium-contaminated soil and acknowledged that there is a small group of persons (approximately 0.1% of the United States population) who currently have a dermal sensitization to Cr(VI) primarily through occupational exposure. Based on published studies of human volunteers, the Panel concluded that a small percentage (less than 5%) of persons already sensitized may respond to Cr(VI) in solution at concentrations above 35 ppm. They decided that a much higher concentration in soil, perhaps 350 ppm Cr(VI), would be necessary to elicit dermatitis because only a fraction of the chromium in soil is soluble. The Panel concluded that it was highly unlikely (if not impossible) for a person to become dermally sensitized to Cr(VI) or Cr(III) at the soil concentrations found in most areas in Hudson County.(ABSTRACT TRUNCATED AT 400 WORDS)     

Human skin penetration of selected model mycotoxins

Dermal exposure data for mycotoxins are very scarce and fragmentary, despite their widespread skin contact and hazard toxicity. In this study, the transdermal kinetics of aflatoxin B1 (AFB1), ochratoxin A (OTA), fumonisin B1 (FB1), citrinin (CIT), zearalenone (ZEA) and T-2 toxin (T-2) were quantitatively evaluated, using human skin in an in vitro Franz diffusion cell set-up. All mycotoxins penetrated through the skin, except for FB1, which showed concentrations in the receptor fluid below the LoD, resulting in a K(p)<3.24×10(-6)cm/h. OTA showed the highest permeation (K(p)=8.20×10(-4)cm/h), followed by CIT (K(p)=4.67×10(-4)cm/h). AFB1 and ZEA showed lower permeability rates (K(p)=2.11 and 2.33×10(-4)cm/h, respectively). T-2 was found to have the lowest permeability (K(p)=6.07×10(-5)cm/h). From literature-based mycotoxin-concentrations, dermal contact surface, exposure time and apparent K(p)'s obtained in this study, the daily dermal exposure (DDE) in two industrial and one residential scenario was estimated. Dermal exposure to the DNA-reactive genotoxic carcinogenic AFB1 can lead to a health risk for agricultural workers which are exposed to a mycotoxin contaminated solution in a worst case situation. For all the other investigated mycotoxins, no significant health risk is calculated after dermal contact in neither agricultural nor residential environments.     

Considerations for the development of health-based surface dust cleanup criteria for beryllium

Abstract

The exposure–response patterns with beryllium sensitization (BeS), chronic beryllium disease (CBD) and lung cancer are influenced by a number of biological and physicochemical factors. Recent studies have suggested dermal exposure as a pathway for BeS. In light of the current non-health-based DOE Beryllium Rule surface criteria, the feasibility of deriving a human health-based surface dust cleanup criteria (SDCC) for beryllium was assessed based on toxicology and health risk factors via all potential routes of exposure. Beryllium-specific and general exposure factors were evaluated, including (1) beryllium physicochemical characteristics, bioavailability and influence on disease prevalence, and (2) chemical dissipation, resuspension and transfer. SDCC for non-cancer (SDCC_NC) and cancer (SDCC_CA) endpoints were derived from a combination of modern methods applied for occupational, residential and building reentry surface dust criteria. The most conservative SDCC_NC estimates were derived for dermal exposure (5–379?μg/100?cm² for 0.1–1% damaged skin and 17–3337?μg/100?cm² for intact skin), whereas the SDCC_CA for inhalation exposure ranged from 51 to 485?μg/100?cm². Considering this analysis, the lowest DOE surface criterion of 0.2?μg/100?cm² is conservative for minimizing exposure and potential risks associated with beryllium-contaminated surfaces released for non-beryllium industrial or public sector use. Although methodological challenges exist with sampling and analysis procedures, data variability and interpretation of surface dust information in relation to anthropogenic and natural background concentrations, this evaluation should provide useful guidance with regard to cleanup of manufacturing equipment or remediation of property for transfer to the general public or non-beryllium industrial facilities.     

Dermal absorption of arsenic from soils as measured in the rhesus monkey.

Regulatory agencies have relied on dermal absorption data for soluble forms of arsenic as the technical basis for specific absorption values that are used to calculate exposure to arsenic in weathered soil. These evaluations indicate that percutaneous absorption of arsenic from soil ranges from 3.2 to 4.5% of the dermally applied dose, based on studies of arsenic freshly mixed with soil. When this value is incorporated into risk assessments and combined with other assumptions about dermal exposures to soil, the conclusion is often that dermal exposure to arsenic from soil may contribute significantly to overall exposure to arsenic in soil. Prior characterization research has indicated that the solubility of arsenic in soil varies, depending on the provenance of the soil, the source of the arsenic, and the chemical interaction of arsenic with other minerals present within the soil matrix. Weathering produces forms of arsenic that are more tightly bound within the soil and less available for absorption. Our research expands on prior in vivo studies to provide insights into the potential for dermal absorption of arsenic from the more environmentally relevant substrate of soil. Specifically, two soils with very high concentrations of arsenic were evaluated under two levels of skin hydration. One soil, containing 1400 mg/kg arsenic, was collected adjacent to a pesticide production facility in New York. The other soil, containing 1230 mg/kg arsenic, was collected from a residential area with a history of application of arsenical pesticides. Although the results of this research are constrained by the small study size dictated by the selection of an animal research model using monkeys, the statistical power was optimized by using a "crossover" study design, wherein each animal could serve as its own comparison control. No other models (animal or in vitro) were deemed adequate for studying the dermal absorption of soil arsenic. Our results show dermal absorption of soluble arsenic in solution to be 4.8 +/- 5.5%, which is similar to results reported earlier for arsenic in solution (and used by regulatory agencies in recommendations regarding dermal absorption of arsenic). Conversely, absorption following application of arsenic in the soil matrices resulted in mean estimated arsenic absorption of 0.5% or less for all soils, and all individual estimates were less than 1%. More specifically, following application of arsenic-bearing soils to the abdomens of monkeys, urinary arsenic excretion could not be readily distinguished from background. This was true across all five soil-dosing trials, including application of the two dry soils and three trials with wet soil. These findings are consistent with our understanding of the environmental chemistry of arsenic, wherein arsenic can be present in soils in complexed mineral forms. This research addresses an important component involved in estimating the true contribution of percutaneous exposures to arsenic in soil relative to exposures via ingestion. Our findings suggest that dermal absorption of arsenic from soil is truly negligible, and that EPA's current default assumption of 3% dermal absorption of arsenic from soils results in significant overestimates of exposure.     

Bioavailability of Soil-Bound TCDD: Dermal Bioavailability in the Rat

Bioavailability of Soil-Bound TCDD: Dermal Bioavailability inthe Rat. SHU, H., TEITELBAUM, T., WEBB, A. S., MARPLE, L., BRUNCK,B. DEI ROSSI, D., MURRAY, J., AND PAUSTENBACH, D. (1988). Fundam.Appl. Toxicol. 10, 335-343. 2,3,7,8-Tetrachlorodibenzo-p-dioxin(TCDD), an unwanted by-product formed during the manufactureof hexachlorophene and phenoxyherbicides, has been found asan environmental contaminant in many U.S. and Western Europeansites. This study examines in the rat the degree of dermal absorptionof TCDD bound to soil. Such information would assist regulatoryagencies in evaluating the degree of exposure of humans whocome in contact with TCDD-contaminated soil. Several parameterswhich may influence dermal absorption were studied, includingTCDD dose, duration of contact, presence of crankcase oil asa co-contaminant, and environmentally contaminated vs laboratory-preparedsoil. The dermal penetration of TCDD following 4 hr of contactwith skin was approximately 60% of that following 24 hr of contact(P 0.05). Following 24 hr of contact with the skin, the degreeof dermal uptake of TCDD contaminated soil was approximately1% of the administered dose. Under the conditions of the presentstudy, the degree of uptake does not appear to be influencedto any significant extent by the concentration of TCDD on soil,the presence of crankcase oil as co-contaminants, or by environmentallyvs laboratory-contaminated soil. Although a number of parametersexamined in this study did not significantly influence the degreeof dermal absorption of TCDD in the rat following 24 hr of contactwith the contaminated soil, the unqualified use of the 1% valueto estimate human exposure would overestimate human exposure,since there is general agreement among researchers that ratskin tends to be more permeable than human skin to highly lipid-solublecompounds such as TCDD.     

Oral and dermal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces cutaneous papillomas and squamous cell carcinomas in female hemizygous Tg.AC transgenic mice.

Tg.AC mice develop epidermal papillomas in response to treatment with dermally applied nongenotoxic and complete carcinogens. The persistent environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a multi-site rodent carcinogen and tumor promoter that induces the formation of papillomas in Tg.AC mice. To examine the dose-response relationship and compare dermal and oral routes of exposure for TCDD-induced skin papillomas, female Tg.AC mice were exposed dermally to average daily doses of 0, 2.1, 7.3, 15, 33, 52, 71, 152, and 326 ng TCDD/kg/day or 0, 75, 321, and 893 ng TCDD/kg body weight by gavage for 26 weeks. The incidence of cutaneous papillomas was increased in a dose-dependent manner, and tumors developed earlier with higher exposure to TCDD regardless of route of administration. Increased incidences of cutaneous squamous cell carcinomas were observed in mice exposed to dermal (> or =52 ng/kg) and oral (893 ng/kg) TCDD. Higher gavage doses than dermal exposure doses were required to induce papillomas and squamous cell carcinomas. Despite a linear correlation between administered dose and terminal skin concentrations, the incidence of tumor formation was lower in the gavage study than in the dermal study with respect to mean terminal skin TCDD concentrations. These studies demonstrate that, although Tg.AC mice are less responsive to TCDD by gavage than by dermal exposure, the induction of skin neoplasms is a response to systemic exposure and not solely a local response at the site of dermal application. Differences in response between the routes of exposure may reflect pharmacokinetic differences in the delivery of TCDD to the skin over the duration of the study.     

Effects of chronic dietary exposure to environmentally relevant concentrations to 2,3,7,8-tetrachlorodibenzo-p-dioxin on survival,growth, reproduction and biochemical responses of female rainbow trout (Oncorhynchus mykiss)

Adult female rainbow trout were exposed to dietary 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at concentrations of 1.8, 18 and 90 ng TCDD/kg (ww) food for up to 300 day. At the end of the exposure fish were spawned and the reproductive outcomes were assessed. TCDD was accumulated into tissues and eggs in a dose-dependent manner with steady state being achieved after 50-100 day of exposure. Biochemical and hematological parameters were monitored at 50, 100, 150, and 200 day after the beginning of exposure. The survival of adult female trout was reduced in a dose-dependent manner by exposure to TCDD in the diet. Fish fed 1.8 ng TCDD/kg, moist weight of diet, showed significantly reduced survival compared with those fed the control diet. TCDD also affected survival of fry from females fed 1.8 ng TCDD/kg. Observed adverse effects in adult fish were as sensitive as early life-stage endpoints. Liver EROD activity was only moderately increased in all exposure groups after 250+ day of exposure. Low rates of edema and deformities were observed in fry from all treatment groups including controls. This study has demonstrated adverse effects of TCDD to both adults and fry at concentrations comparable to current environmental concentrations. This suggests that direct adult toxicity as well as reproductive endpoints need to be incorporated in the current risk assessment paradigm for these compounds.     

Dietary exposure to 3,3',4,4',5-pentachlorobiphenyl (PCB 126) or 2,3,7,8-tetrachlorodibenzo-p-dixon (TCDD) does not induce proliferation of squamous epithelium or osteolysis in the jaws of weanling rats

Previous studies demonstrated that dietary exposure to 24 ppb 3,3',4,4',5-pentachlorobiphenyl (PCB 126) or 2.4 ppb 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced maxillary and mandibular proliferation of periodontal squamous epithelium, osteolysis of alveolar bone, and loose and displaced teeth in juvenile mink (Mustela vison). This study determined if such effects could be induced in laboratory rats. Feeding weanling male Long Evans rats 20 or 100 ppb PCB 126 or 1 or 10 ppb TCDD for up to 101 days caused a dose-dependent decrease in body weight gains but did not produce the jaw lesion observed in PCB 126- or TCDD-treated mink.     

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.     

Selenium and human health implications in California's San Joaquin Valley

An evaluation was conducted on the human health impacts of elevated levels of selenium in the Kesterson National Wildlife Refuge and its surroundings in Merced County, California. Investigative activities of various agencies were summarized and assessed. Agricultural waste water not intended for human use showed elevated selenium concentrations of up to 1400 ppb. Levels of selenium in fish (up to 96 ppm, wet weight), aquatic birds (up to 130 ppm in liver, dry weight), and waterfowl (up to 5.3 ppm flesh, wet weight) were unsafe for unrestricted human consumption. Data on selenium in drinking water (less than 10 ppb), animals (mean values: beef liver 0.3-0.35 ppm, wet weight; milk, 0.01-0.02 ppm), and air (particulate, 14.8 ng/m3; gaseous, less than 1080 ng/m3) did not suggest a high level of exposure. Selenium concentrations in soil were highly variable and suggested a potential source of high exposure. Selenium values in blood and urine of workers were within normal range. A community health survey did not show any trend of adverse health effects in the local population.     

Ingestion of Soil Contaminated with 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Alters Hepatic Enzyme Activities in Rats

Ingestion of Soil Contaminated with 2,3,7,8-Tetrachlorodibenzo-p-dioxin(TCDD) Alters Hepatic Enzyme Activities in Rats. LUCIER, G.W., RUMBAUGH, R. C., MCCOY, Z., HASS, R., HARVAN, D., AND ALBRO,P. (1986). Fundam. Appl. Toxicol. 6, 36.4–371. Femalerats were treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)in either corn oil or contaminated soil from the Minker sitein Missouri. Eight doses ranging from 0.015 to 5 µg TCDD/kgwere used in the corn oil group; the range was 0.015 to 5.5TCDD/kg in the TCDD-contaminated soil group. Rats in a thirdgroup were given equal amounts of soil uncontaminated with TCDD.No acute toxicity or effects on body weight gain were observedat these doses. In general, equivalent doses of TCDD in cornoil or TCDD in soil produced similar increases in hepatic arylhydrocarbon hydroxylase activity (AHH) and UDP glucuronyltransferaseactivity although effects were slightly greater in the TCDD–cornoil groups. In the corn oil groups, the induction of AHH rangedfrom about 30-fold at the highest dose to twofold at the lowestdose studied. TCDD also caused an increase in cytochrome P-450concentration and a shift in spectral peak from 450 to 448 nm.There was no effect of TCDD on ethylmorphine N-demethylase,consistent with previous reports. Liver concentrations of TCDD(mean ± SD) in the 5-µg/kg groups were 40.8 ±6.3 ppb in the TCDD- corn oil group and 20.3 ± 12.9 ppbin the TCDD-contaminated soil group. Our results suggest thatthe bioavailability of TCDD in soil in rats is approximately50%. Therefore, ingestional exposure to TCDD-contaminated soilmay constitute a significant health hazard in view of its extremelyhigh toxicity and relatively high bioavailability.     

Health risk assessment and source apportionment of PAHs in industrial and bitumen contaminated soils of Kermanshah province; NW Iran

A comprehensive study conducted for investigating the presence of polycyclic aromatic hydrocarbons (PAHs) in bitumen contaminated (BC) and industrial contaminated (IC) soils of Kermanshah province to evaluate their sources and health risk assessment. Forty-two surface soil (0-30 cm) samples were collected and analyzed for 16 PAHs. The total PAHs concentrations, show a mean value of 31.33 mg/kg and 56.31 mg/kg, ranging from 7.35 to 291.38 mg/kg and 6.59 to 662.83 mg/kg in BC and IC soil samples respectively. Positive matrix factorization model (PMF) was used to investigate the source apportionment of PAHs. PMF analysis identified four sources of PAHs as; fossil fuel combustion and unburned petroleum (28.76%), biomass/coal burning (23.55%), vehicular emissions (23.67%) and creosotes (24.01 %) in BC soils and biomass combustion (44.11%), unburned petroleum and coal combustion (17.54%), fossil fuel combustion (19.02%) and creosotes (19.32 %) in IC soils. Ecological risk assessment of PAHs showed that all of the PAHs levels are higher than the effects range low (ERL) values, except for benzo( a)anthracene. Three rings and fluoranthene of the PAHs in IC soils and Nap, Acy, Ace, Phe, Ant, Flt and DBA in BC soil samples reveal higher concentrations than the effects range median (ERM) values. Benzo( a)pyrene equation (BaP_eq) values indicate that the carcinogenic potency of PAHs should be given more awareness due to impending environmental risk in the study area. The total incremental life time cancer risk (ILCR) of exposure to PAHs is 9.21×10^-3 for adult and 9.54×10^-3 for children in BC soil samples and 1.13×10^-2 for adult and 1.17×10^-2 for children in IC soil samples. Estimated results of ILCR indicate that soil samples are potentially exposed to high cancer risk via both ingestion and dermal contact.     

Percutaneous absorption of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) from soil

Eight dermal absorption experiments (two in vivo; six in vitro) and one intravenous experiment were conducted using 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) either neat (high dose at approximately 250 microg/cm(2) and low dose at 10 ng/cm(2)) or sorbed on a low organic soil (LOS) or high organic soil (HOS) at 1 ppm (10 ng TCDD/10 mg soil/cm(2)). After 96 h the percent of applied dose absorbed (PADA) for the neat low dose was 78% in vivo (rat) and 76% in vitro (rat). PADA for the equivalent TCDD dose sorbed on LOS were 16.3% (rat in vivo), 7.7% (rat in vitro) and 2.4% (human in vitro). The PADA for TCDD sorbed on HOS (1 ppm) was 1.0% (rat in vitro). Generally, rat skin was observed to be three to four times more permeable to TCDD than human skin. At steady state, the dermal flux of TCDD in neat form, sorbed on LOS at 1 ppm, and sorbed on HOS at 1 ppm (all in vitro, rat) was 120, 0.007, and 0.0007 ng/cm(2)/h, respectively (ratio = 1.7 x 10(5):10:1). Making adjustments to account for differences between in vitro and in vivo results and adjusting for application to monolayer loads, the 24-h TCDD absorption for human skin is estimated as 1.9% from LOS (1 ppm) and 0.24% from HOS (1 ppm).     

The Effect of Perinatal Exposure to Tetrachlorodibenzo-p-Dioxin on the Immune Response of Young Mice

ABSTRACT

The immunocompetence of 5 week old offspring from mice fed control chow or chow containing 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was evaluated. The 5 ppb maternal feeding level was the only level that produced symptoms of intoxication in the offspring (i.e., facial alopecia and periorbital edema). Mice from mothers fed either 2.5 or 5 ppb of TCDD demonstrated thymus cortex atrophy and a significantly reduced spleen anti-SRBC plaque forming cell (PFC) response, but had normal serum anti-SRBC antibody levels following primary and secondary immunization. Contact sensitivity response to DNFB was significantly reduced only in offspring from mothers fed 5 ppb of TCDD. The blastogenio response of splenic T- and B-lymphocytes to concanavalin-A and E. coli lipopolysaccharide was unaffected by perinatal TCDD exposure. This correlated with the normal appearance of the T- and B-cell dependent areas of the spleens from these animals. There was no significant difference in the differential white blood cell counts between control and TCDD-exposed offspring. Offspring from mothers fed up to 5 ppb of TCDD withstood a live Listeria challenge as well as controls. However, maternal feeding levels as low as 1 ppb of TCDD rendered offspring more sensitive to an endotoxin challenge.