PubMed Health⌕ Search

Biomedical subjects

D J Paustenbach

Publications and source records attributed to D J Paustenbach.

At least 19 recordsLinked to original sources
PubMed2004

Estimating historical occupational exposure to airborne hexavalent chromium in a chromate production plant: 1940--1972.

This article presents a retrospective exposure assessment for 493 workers who were occupationally exposed to airborne hexavalent chromium, Cr(VI), at a Painesville, Ohio, chromate production plant from 1940-1972. Exposure estimates were reconstructed using a job-exposure matrix approach that related job titles with area monitoring data from 21 industrial hygiene surveys conducted from 1943 to 1971. No personal monitoring data were collected. Specifically, airborne Cr(VI) concentration profiles for 22 areas of the plant, termed job-exposure group (JEG) areas, were constructed for three distinct time periods (1940-1949, 1950-1964, and 1965-1972), with cut points based on known major plant and process changes. Average airborne Cr(VI) concentrations were the highest for the bridge crane operators (5.5 mg/m3) prior to 1965, although only four cohort members held this job title. Airborne concentrations for the rest of the production areas of the plant ranged from 1.9 mg/m3 for packers in the 1940s to 0.012 mg/m3 for ore mill operators after 1964. For nearly all JEG areas, exposures decreased over time, particularly after 1964. For example, average airborne concentrations in production areas of the plant decreased from 0.72 mg/m3 in the 1940s to 0.27 mg/m3 from 1950 to 1964, and the average was 0.039 mg/m3 after 1964. Former workers were interviewed to determine activity patterns in the plant by job title. This information was combined with Cr(VI) monitoring data to calculate cumulative occupational exposure for each worker. Cumulative exposures ranged from 0.003 to 23 (mg/m3) x years. The highest monthly 8-hour average exposure concentration for each worker ranged from 0.003 to 4.1 mg/m3. These exposure estimates have been combined with mortality data for this cohort to assess the lung cancer risk associated with inhaled Cr(VI), and a positive dose-response relationship was observed for increases in lung cancer mortality with measures of cumulative exposure and highest monthly exposure.

Air Pollution, Indoor↗
PubMed2003

Workplace airborne hexavalent chromium concentrations for the Painesville, Ohio, chromate production plant (1943-1971).

Hexavalent chromium [Cr(VI)] is recognized as an inhalation carcinogen, based primarily on the increased incidence of lung cancer among occupationally exposed workers. To assess the carcinogenic potency of Cr(VI), both the U.S. Environmental Protection Agency and the Occupational Safety and Health Administration have relied on data from a 1930s cohort of workers from the Painesville, Ohio, chromate production plant. However, the exposure information for this cohort has several shortcomings. In an effort to provide better exposure information, we present here recently identified historical exposure data for the Painesville workers. More than 800 measurements of airborne Cr(VI) from 23 newly identified surveys conducted from 1943 to 1971 are presented. The results indicate that the highest Cr(VI) concentrations recorded at the plant occurred in shipping (e.g., bagging of dichromate), lime and ash, and filtering operations, with maximum yearly average Cr(VI) concentrations of 8.9, 2.7, and 2.3 mg/m(3), respectively. The locker rooms, laboratory, maintenance shop, and outdoor raw liquor storage areas had the lowest average Cr(VI) air concentrations over time, with yearly average concentrations that rarely exceeded the historical and current Threshold Limit Value TLV(R) of 0.05 mgCr(VI)/m(3) (0.1 mgCrO(3)/m(3)). Concentrations generally decreased in the plant over time. The average airborne concentration of Cr(VI) in the indoor operating areas of the plant in the 1940s was 0.72 mg/m(3), that from 1957 through 1964 was 0.27 mg/m(3), and that from 1965 through 1972 was 0.039 mg/m(3). Although in some ways limited, these data are of sufficient quality to allow for exposure reconstruction for workers employed at this plant from 1940 to 1972, and to provide the basis for an improved cancer risk assessment.

Air Pollutants, Occupational↗
PubMed2002

Oral bioaccessibility of dioxins/furans at low concentrations (50-350 ppt toxicity equivalent) in soil.

Animal studies have indicated that the oral bioavailability of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in environmentally contaminated soil could range from 0.5 to 60%. To estimate the oral bioavailability of TCDD, and the 16 other 2,3,7,8-substituted dioxin/furan congeners, this study used a physiologically based extraction test, designed around the anatomic and physiologic characteristics of the human digestive tract. This test measures the fraction of dioxins/furans in soil that would be solubilized in the gastrointestinal tract (i.e., that would be bioaccessible) and therefore available for absorption. Eight soils from Midland, MI, were evaluated in this study and exhibited TCDD concentrations of 1.7-139 pg/g (ppt) and total TEQ concentrations of 6-340 ppt. Bioaccessibility of dioxins/furans from these soils ranged from 19 to 34% averaged across the 17 2,3,7,8-substituted dioxin/furan congeners), with an average of 25%. The total organic carbon in these soils was low--ranging from 1 to 4%--particularly for the soil series from which they were collected. Bioaccessibility of individual congeners did not appear to be correlated with degree of chlorination. Even though these dioxin/furan concentrations are much less than studied previously, these results are consistent with those from animal studies at other sites, which have generally yielded values of 20-60% relative bioavailability for TCDD in soil.

Absorption↗
PubMed2001

An event-by-event probabilistic methodology for assessing the health risks of persistent chemicals in fish: a case study at the Palos Verdes Shelf.

A human health risk assessment of recreational anglers who consume fish from the Palos Verdes Shelf was conducted. The uptake of DDT, DDE, and DDD (collectively total DDT or tDDT) and polychlorinated biphenyls (PCBs) due to fish ingestion was characterized using Monte Carlo techniques. This analysis relied upon 176 probability density functions developed from over 300,000 individual pieces of information to represent 17 different exposure factors that influence the human uptake of persistent organic chemicals in fish. The carcinogenic and noncarcinogenic risks were estimated using a microexposure event modeling approach that estimates exposure on an event-by-event basis. This evaluation relied upon several large studies that provided site-specific data on angler behavior and concentratioins of chemicals in 13 fish species. Our results indicate that the median theoretical increased lifetime cancer risk associated with estimated exposure to tDDT and PCBs was 5 x 10(-8) for anglers who fish on commercial passenger fishing vessels (CPFVs) and who catch and eat fish from the Palos Verdes Shelf. The mean risk for these anglers was 2 x 10(-7), and the 95th percentile risk was 8 x 10(-7). At the 9.5th percentile, the hazard quotients for anglers were less than 1, indicating that noncancer effects are unlikely. These results are in contrast with prior risk assessments of this site that suggested that consumption of white croaker alone posed a cancer risk of 2 x 10(-3) and a hazard quotient of 32. Our results were validated by their agreement with several independent local studies regarding fishing and consumption practices. This assessment indicates that the levels of tDDT and PCB in fish at the Palos Verdes Shelf do not pose a significant risk to human health among recreational anglers. Based on the size of the local angler population, no cases of cancer would be expected to result from eating Palos Verdes Shelf fish. The methodology used here should be applicable to characterizing the risks to those who ingest fish from the waterways of most industrialized nations.

Animals↗
PubMed2001

A comparison and critique of historical and current exposure assessment methods for beryllium: implications for evaluating risk of chronic beryllium disease.

The primary beryllium industry has generated a large amount of data on airborne beryllium concentrations that has been used to characterize exposure by task-specific activities, job category, individual worker, and processing area using a variety of methods. These methods have included high-volume breathing zone sampling, high-volume process sampling, high- and low-volume respirable and area sampling, real-time monitoring, and personal sampling. Many of the beryllium studies have used these air sampling methods to assess inhalation exposure and chronic beryllium disease (CBD) risk to beryllium; however, available data do not show a consistent dose-response relationship between airborne concentrations of beryllium and the incidence of CBD. In this article, we describe the air sampling and exposure assessment methods that have been used, review the studies that have estimated worker exposures, discuss the uncertainties associated with the level of beryllium for which these studies have reported an increased risk of CBD, and identify future investigative exposure assessment strategies. Our evaluation indicated that studies of beryllium workers are often not directly comparable because they (1) used a variety of exposure assessment methods that are not necessarily representative of individual worker exposures, (2) rarely considered respirator use, and (3) have not evaluated changes in work practices. It appears that the current exposure metric for beryllium, total beryllium mass, may not be an appropriate measurement to predict the risk of CBD. Other exposure metrics such as mass of respirable particles, chemical form, and particle surface chemistry may be more related to the prevalence of CBD than total mass of airborne beryllium mass. In addition, assessing beryllium exposure by all routes of exposure (e.g., inhalation, dermal uptake, and ingestion) rather than only inhalation exposure in future studies may prove useful.

Air Pollutants, Occupational↗
PubMed2001

Contribution of incidental exposure pathways to total beryllium exposures.

Beryllium manufacturing processes are associated with the immune-mediated chronic beryllium disease (CBO). Recent workplace epidemiological studies have been relatively unsuccessful in correlating disease with workplace air concentrations of beryllium, thereby failing to support the hypothesis that dose by the respiratory route determines the risk of disease. This has led to consideration of the hypotheses that dermal or oral exposures to beryllium can influence disease risk, either as a cause of sensitization or to induced tolerance to beryllium. If so, the control of dermal and/or ingestion exposure to beryllium, which has heretofore been widely disregarded in the United States, would be of practical importance. Most of the literature of the past 50 years indicates that ingestion and dermal uptake of beryllium are unimportant routes of exposures. The toxicology data generally support this position. However, research is under way to determine whether sensitization to beryllium may occur following exposure via routes other than inhalation, raising the question of whether this sensitization from other routes of exposure makes the lungs more susceptible to inflammation when inhaled doses are encountered. Using published data on other metals, this article describes the likely range of doses that a worker might incur in the workplace due to incidental exposure pathways (i.e., exposures not directly related to inhalation of workplace air), such as hand-to-mouth exposure, dermal contact, and resuspension following deposition of beryllium onto clothing. This analysis indicates that these incidental routes of exposure could contribute to total absorbed doses of beryllium that exceed simple airborne inhalation exposures. Because the doses presented by these alternative exposure pathways could be appreciable compared with the airborne inhaled dose, and could continue even when respirators are worn, these pathways may represent the primary routes of entry of beryllium into the body. We believe that the potential for exposure from these incidental exposure pathways merits additional study.

Administration, Oral↗
PubMed2001

Identifying an apppropriate occupational exposure limit (OEL) for beryllium: data gaps and current research initiatives.

The occupational exposure limit of 2.0 microg/m3 for beryllium has been used in the workplace since the late 1940s. In particular, the adequacy of the American Conference of Governmental Industrial Hygienists (ACGIH) Threshold Limit Value (TLV) for beryllium has recently come into question. The symposium "Beryllium: Effect on Worker Health" was convened in September 1999, to bring together leading scientists to present and discuss current research activities on beryllium exposure and chronic beryllium disease (CBD). One of the key questions to be resolved at the symposium was, "Is there a sufficient understanding of exposure and the cause of CBD that would allow us to develop a TLV that we believe would prevent disease?" Seven scientists presented information regarding the current understanding of the disease, possible causes, and ongoing research. The topics were (1) biomonitoring approaches and their relationship with clinical effects, (2) historical and current exposure assessments, (3) sampling methods and aerosol characterization, and (4) epidemiology. Six basic hypotheses regarding the relationship between exposure to beryllium and CBD were generated from the information presented at the symposium. The six hypotheses that are related to issues such as beryllium form, particle size, industrial hygiene practices, extrapulmonary routes of exposure, and genetic susceptibility also appear to be the focus of ongoing and likely future research initiatives. This article summarizes both the presentations made at the meeting and the hypotheses generated. It is expected that an understanding of these issues should explain the inconsistent dose-response relationship observed between exposure and CBD. The ongoing and planned research is anticipated to provide sufficient data within two to three years to develop one or more scientifically sound TLVs for the different chemical forms of beryllium.

Air Pollutants, Occupational↗
PubMed2001

A physiologically based model for the ingestion of chromium(III) and chromium(VI) by humans.

A physiologically based model of human chromium kinetics has been developed, based on an existing physiologically based model of human body and bone growth (O'Flaherty, 1993, Toxicol. Appl. Pharmacol. 118, 16-29; 1995a, Toxicol. Appl. Pharmacol. 131, 297-308; 2000, Toxicol. Sci. 55, 171-18) and an existing physiologically based model of chromium kinetics in rats (O'Flaherty, 1996, Toxicol. Appl. Pharmacol. 138, 54-64). Key features of the adapted model, specific to chromium, include differential absorption of Cr(VI) and Cr(III), rapid reduction of Cr(VI) to Cr(III) in all body fluids and tissues, modest incorporation of chromium into bone, and concentration-dependent urinary clearance consistent with parallel renal processes that conserve chromium efficiently at ambient exposure levels. The model does not include a physiologic lung compartment, but it can be used to estimate an upper limit on pulmonary absorption of inhaled chromium. The model was calibrated against blood and urine chromium concentration data from a group of controlled studies in which adult human volunteers drank solutions generally containing up to 10 mg/day of soluble inorganic salts of either Cr(III) (chromic chloride, CrCl(3)) or Cr(VI) (potassium dichromate, K(2)Cr(2)O(7)) (Finley et al., 1997, Toxicol. Appl. Pharmacol. 142, 151-159; Kerger et al., 1996, Toxicol. Appl. Pharmacol. 141, 145-158; Paustenbach et al., 1996, J. Toxicol. Environ. Health 49, 453-461). In one of the studies, in which the chromium was ingested in orange juice, urinary clearance was observed to be more rapid than when inorganic chromium was ingested. Chromium kinetics were shown not to be dependent on the oxidation state of the administered chromium except in respect to the amount absorbed at these ambient and moderate-to-high exposures. The fraction absorbed from administered Cr(VI) compounds was highly variable and was presumably strongly dependent on the degree of reduction in the gastrointestinal tract, that is, on the amount and nature of the stomach contents at the time of Cr(VI) ingestion. The physiologically based model is applicable to both single-dose oral studies and chronic oral exposure, in that it adequately reproduced the time dependence of blood plasma concentrations and rates of urinary chromium excretion in one of the subjects who, in a separate experiment, ingested daily 4 mg of an inorganic Cr(VI) salt in 5 subdivided doses of 0.8 mg each for a total of 17 days. The high degree of variability of fractional absorption of Cr(VI) from the gastrointestinal tract leads to uncertainty in the assignment of a meaningful value to this parameter as applied to single Cr(VI) doses. To model chronic oral chromium exposure at ambient or moderately above-ambient levels, the physiologically based model in its present form should be usable with urinary clearance set to a constant value of 1-2 liters/day and the gastrointestinal absorption rate constants set at 0.25/day for Cr(III) and 2.5/day for Cr(VI). The model code is given in full in the Appendix.

Administration, Oral↗
PubMed2001

Proposed occupational exposure limits for select ethylene glycol ethers using PBPK models and Monte Carlo simulations.

Methoxyethanol (ethylene glycol monomethyl ether, EGME), ethoxyethanol (ethylene glycol monoethyl ether, EGEE), and ethoxyethyl acetate (ethylene glycol monoethyl ether acetate, EGEEA) are all developmental toxicants in laboratory animals. Due to the imprecise nature of the exposure data in epidemiology studies of these chemicals, we relied on human and animal pharmacokinetic data, as well as animal toxicity data, to derive 3 occupational exposure limits (OELs). Physiologically based pharmacokinetic (PBPK) models for EGME, EGEE, and EGEEA in pregnant rats and humans have been developed (M. L. Gargas et al., 2000, Toxicol. Appl. Pharmacol. 165, 53-62; M. L. Gargas et al., 2000, Toxicol. Appl. Pharmacol. 165, 63-73). These models were used to calculate estimated human-equivalent no adverse effect levels (NAELs), based upon internal concentrations in rats exposed to no observed effect levels (NOELs) for developmental toxicity. Estimated NAEL values of 25 ppm for EGEEA and EGEE and 12 ppm for EGME were derived using average values for physiological, thermodynamic, and metabolic parameters in the PBPK model. The uncertainties in the point estimates for the NOELs and NAELs were estimated from the distribution of internal dose estimates obtained by varying key parameter values over expected ranges and probability distributions. Key parameters were identified through sensitivity analysis. Distributions of the values of these parameters were sampled using Monte Carlo techniques and appropriate dose metrics calculated for 1600 parameter sets. The 95th percentile values were used to calculate interindividual pharmacokinetic uncertainty factors (UFs) to account for variability among humans (UF(h,pk)). These values of 1.8 for EGEEA/EGEE and 1.7 for EGME are less than the default value of 3 for this area of uncertainty. The estimated human equivalent NAELs were divided by UF(h,pk) and the default UFs for pharmacodynamic variability among animals and among humans to calculate the proposed OELs. This methodology indicates that OELs (8-h time-weighted average) that should protect workers from the most sensitive adverse effects of these chemicals are 2 ppm EGEEA and EGEE (11 mg/m(3) EGEEA, 7 mg/m(3) EGEE) and 0.9 ppm (3 mg/m(3)) EGME. These recommendations assume that dermal exposure will be minimal or nonexistent.

Administration, Inhalation↗
PubMed2000

A toxicokinetic study of inhaled ethylene glycol ethyl ether acetate and validation of a physiologically based pharmacokinetic model for rat and human.

The solvents ethylene glycol monoethyl ether acetate (EGEEA) and ethylene glycol monoethyl ether (EGEE), at sufficiently high doses, are known to be rodent developmental toxicants, exerting their toxic effects through the action of their metabolite 2-ethoxyacetic acid (2-EAA). Thus risks associated with exposure to these compounds are best evaluated based on a measure of the internal dose of 2-EAA. The goals of the work reported here were to develop physiologically based pharmacokinetic (PBPK) models of EGEEA and EGEE for pregnant rats and humans. These models were used to identify human exposure levels (ppm in air) equivalent to the rat no observed effect level (NOEL) and lowest observed effect level (LOEL) for developmental effects (Hanley et al., 1984). We exposed pregnant Sprague-Dawley rats to concentrations of EGEEA corresponding to the NOEL and LOEL. Maternal blood, urine, and fetal tissue concentrations of EGEE and 2-EAA measured in these experiments were used to validate the rat EGEEA and EGEE models. Data collected by other researchers were used to validate the capabilities of the rodent EGEEA and EGEE models to predict the kinetics in humans. The models for estimating circulating blood concentrations of 2-EAA were considered valid based on the ability of the model to accurately predict 2-EAA concentrations in rat blood, urine, and fetal tissue. The human inhaled concentration equivalent to the rat NOEL for EGEEA (50 ppm) was predicted to be 25 ppm using the maternal blood average daily area under the curve (AUC) and 40 ppm using the maximum concentration achieved in maternal blood (C(max)). The human inhaled concentration equivalent to the rat LOEL for EGEEA (100 ppm) was determined to be 55 ppm using the maternal blood average daily AUC and 80 ppm using the maternal blood C(max).

Animals↗
PubMed2000

A toxicokinetic study of inhaled ethylene glycol monomethyl ether (2-ME) and validation of a physiologically based pharmacokinetic model for the pregnant rat and human.

Exposures to sufficiently high doses of ethylene glycol monomethyl ether (2-methoxyethanol, 2-ME) have been found to produce developmental effects in rodents and nonhuman primates. The acetic acid metabolite of 2-ME, 2-methoxyacetic acid (2-MAA), is the likely toxicant, and, as such, an understanding of the kinetics of 2-MAA is important when assessing the potential risks to humans associated with 2-ME. A previously described physiologically based pharmacokinetic (PBPK) model of 2-ME/2-MAA kinetics for rats exposed via oral or iv administration was extended and validated to inhalation exposures. Pregnant Sprague-Dawley rats were exposed for 5 days (gestation days 11-15), 6 h/day, to 2-ME vapor at 10 and 50 ppm. Validation consisted of comparing model output to maternal blood and fetal 2-ME and 2-MAA concentrations during and following 5 days of exposure (gestation days 11-15). These concentrations correspond to a known no observed effect level (NOEL) and a lowest observed effect level (LOEL) for developmental effects in rats. The rat PBPK model for 2-ME/2-MAA was scaled to humans and the model (without the pregnancy component) was used to predict data collected by other investigators on the kinetics of 2-MAA excretion in urine following exposures to 2-ME in human volunteers. The partially validated human model (with the pregnancy component) was used to predict equivalent human exposure concentrations based on 2-MAA dose measures (maximum blood concentration, C(max), and average daily area under the 2-MAA blood concentration curve, AUC, during pregnancy) that correspond to the concentrations measured at the rat NOEL and LOEL exposure concentrations. Using traditional PBPK scale-up techniques, it was calculated that pregnant women exposed for 8 h/day, 5 days/week, for the duration of pregnancy would need to be exposed to 12 or 60 ppm 2-ME to produce maternal 2-MAA blood concentrations (C(max) or average daily AUC) equivalent to those in rats exposed to the NOEL (10 ppm) or LOEL (50 ppm), respectively.

Acetates↗
PubMed2000

Assessment of airborne exposure to trihalomethanes from tap water in residential showers and baths.

This study evaluates airborne concentrations of common trihalomethane (THM) compounds in bathrooms during showering and bathing in homes supplied with chlorinated tap water. Three homes in an urban area were selected, each having three bedrooms, a full bath, and approximately 1,000 square feet of living area. THMs were concurrently measured in tap water and air in the shower/bath enclosure and the bathroom vanity area using Summa canisters. Chloroform (TCM), bromodichloromethane (BDCM), and chlorodibromomethane (CDBM) were quantified using U.S. Environmental Protection Agency (EPA) Method TO-14. Air samples were collected prior to, during, and after the water-use event for 16 shower and 7 bath events. Flow rate and temperature were measured, but not controlled. The increase in average airborne concentration (+/- standard error) during showers (expressed as microg/m3 in shower enclosure or bathroom air per microg/L in water) was 3.3+/-0.4 for TCM, 1.8+/-0.3 for BDCM, and 0.5+/-0.1 for CDBM (n = 12), and during baths was 1.2+/-0.4 for TCM, 0.59+/-0.21 for BDCM, and 0.15+/-0.05 for CDBM (n = 4). The relative contribution of each chemical to the airborne concentrations was consistent for all shower and bath events, with apparent release of TCM > BDCM > CDBM. The results are therefore consistent with their relative concentration in tap water and their vapor pressures. When the shower findings for TCM are normalized for water concentration, flow rate, shower volume, and duration, the average exposure concentrations in these urban residences are about 30% lower than those reported by other investigators using EPA analytical methods. This difference is likely attributable primarily to greater air exchange rates in residential shower/bath stalls compared to more "airtight" laboratory shower chambers. This appears to be the first field study to thoroughly evaluate THM exposures from residential showers and baths, and can be used to validate previously published models of tap water volatile chemical transfer to indoor air.

Adult↗
PubMed1999

An environmental hazard assessment of low-level dermal exposure to hexavalent chromium in solution among chromium-sensitized volunteers.

To evaluate the potential for elicitation of allergic contact dermatitis from contact with standing water in the environment, 26 persons known to be allergic to hexavalent chromium [Cr(VI)] were exposed to 25 to 29 mg/L Cr(VI) by immersion of one arm for 30 minutes per day on 3 consecutive days in a potassium dichromate bath. Sixteen of the 26 volunteers demonstrated either no or an equivocal response to the Cr(VI) challenge. Ten of the volunteers developed a few papules or vesicles (1 to approximately 15), mild redness, and pruritus on the Cr(VI)-challenged arm. Histopathological examination of the papules revealed spongiosis and perieccrine and perivascular inflammation. The responses were diagnosed as acute perieccrine reactions. It was concluded that exposure to similar concentrations of Cr(VI) in the environment does not pose an allergic contact dermatitis hazard, even to Cr-sensitized persons.

Biopsy↗
PubMed1998

The prevalence of chromium allergy in the United States and its implications for setting soil cleanup: a cost-effectiveness case study.

Hexavalent chromium [Cr(VI)] elicits allergic contact dermatitis (ACD) among previously sensitized individuals, and some regulatory agencies have suggested the need for Cr(VI) soil standards that are protective of this health end point. To assess the cost effectiveness of implementing ACD-based standards, it is necessary to understand the prevalence of Cr(VI) sensitivity in the general population. More than 30 published studies from 1950 to 1997 were reviewed to determine the prevalence of Cr(VI) sensitivity. No random survey of the general United States (U.S.) population has been performed to date, but the prevalence of Cr(VI) sensitization among North American clinical cohorts (e.g., patients of dermatological clinics) was reported to be 1% in 1996. The prevalence of Cr(VI) sensitivity among the general U.S. population is estimated to be 0.08%. This estimate was calculated by dividing the current U.S. clinical prevalence estimate (1%) by the ratio of Cr(VI) sensitization in clinical vs general populations in The Netherlands (12). A retrospective cost/benefit analysis for sites in Jersey City, New Jersey, suggests that remediation of soils to protect against elicitation of ACD in sensitized individuals is not a cost-effective use of public health resources.

Carcinogens, Environmental↗
PubMed1997

Preliminary assessment of PCB risks to human and ecological health in the lower Passaic River.

Concentrations of Aroclor mixtures and specific polychlorinated biphenyl (PCB) congeners were measured in surface sediments and aquatic biota (striped bass fillet, mummichog, and blue crab muscle and hepatopancreas) collected from the lower Passaic River. Several of the 47 surface sediment samples contained Aroclor concentrations that exceeded a National Oceanic and Atmospheric Administration (NOAA) benchmark level for "total PCBs" (22.7 micrograms/kg). Each of the 18 PCB congeners analyzed in aquatic biota was detected in one or more tissue samples, and numerous congeners were detected in every sample (IUPAC numbers 77, 105, 114, 118, 123, 126, 156, 157, 167, and 189). PCB congener concentrations were similar to those that have been reported in fish from other waterways that contain elevated levels of PCBs. Congener 118 was present at the highest concentration in almost all samples, and constituted 14-60% of the total PCB mass (sum of all congener masses) measured in any given tissue sample. In spite of the prevalence of PCB congeners in biota tissues (up to 1314 micrograms/kg total PCBs), Aroclors were not detected in bass or crab samples at a limit of detection of 33-55 micrograms/kg. This anomaly may be due to selective degradation of certain PCB congeners that are used to analytically recognize and quantitate Aroclors. Using the measured sediment concentrations, a food web model accurately predicted blue crab muscle concentrations of individual PCB congeners (typically within a factor of two) and was also fairly accurate for mummichog (typically within an order of magnitude). Concentrations in striped bass fillet were underestimated by factors of approximately 20-140. Increased cancer risk estimates associated with fish and crab consumption were obtained using four different methods. Using Aroclor tissue concentrations (one-half the limit of detection) and an Aroclor slope factor, total risks were 2.6 x 10(-6); using the "total PCB" measurements and an Aroclor slope factor, total risks were 1.9 x 10(-5); the "PCB-TEQ" method yielded total risks of 6.5 x 10(-4); and USEPA's recent suggested approach for evaluating "dioxin-like" and non-"dioxin-like" effects resulted in a total risk of 6.6 x 10(-4). This wide range in risk estimates indicates that it is critical to the risk management decision-making process that data requirements and risk assessment objectives be carefully evaluated early in the investigation process.

Animals↗
PubMed1997

Urinary chromium as a biological marker of environmental exposure: what are the limitations?

Public concern has mounted recently about environmental exposures to chromium in soil, tap water, and ambient air. In response, agencies charged with protecting public health have attempted to study exposure by monitoring urinary chromium levels among potentially exposed populations. While urinary biomonitoring of occupationally exposed workers has been successfully used to assess high-level inhalation exposures in the workplace, evaluating low-level environmental exposures has been problematic. Due to these problems, before an extensive biological monitoring study is conducted of those exposed to low levels of environmental chromium, several issues must be resolved. First, exposures to chromium must occur at the same time as sampling, because the biological half-life of chromium in urine is very short (less than 2 days). Second, reduced bioavailability and bioaccessibility via the oral and dermal routes of exposure limit the capacity of urinary monitoring to measure environmental exposures (e.g., systemic dose is too small to be measured). Third, the dose of chromium must be sufficient such that it may be reliably measured above background levels in urine (range of 0.2 to 2 microg/liter) and above the analytical limit of detection (0.2 microg/liter). Fourth, the inter- and intrapersonal variability in background levels of urinary chromium is known to be significant and influenced by food and beverage intake, smoking, and exercise. Thus, the role of each factor must be carefully understood. Finally, it is imperative to have developed a complete understanding of the clinical significance of elevated urinary chromium levels before a study is performed, because higher than background levels, in and of themselves, are not indicative of a significant health concern. The route of exposure, valence of chromium to which people were exposed, exposure time, and duration must all be understood before the biological data can be implemented. We have conducted a total of nine human exposure studies over the past 3 years in an attempt to understand the kinetics of chromium and the impact on urinary, red blood cell (RBC), and plasma biomonitoring programs. The results of these studies are described here and our recommendations are offered for how to design and implement a urinary chromium biomonitoring study. In our view, given some evidence that the dose of hexavalent chromium [Cr(VI)] is sufficient to be measurable above background concentrations of total chromium [Cr(III) and Cr(VI)], duplicated measurements of chromium in plasma and RBCs are, in most cases, a more definitive gauge of environmental exposure than urinary biomonitoring.

Biological Availability↗
PubMed1997

Human ingestion of chromium (VI) in drinking water: pharmacokinetics following repeated exposure.

Regulatory agencies have established safe drinking water concentrations for hexavalent chromium [Cr(VI)] based in part on the presumed capability of human gastric juices to rapidly reduce Cr(VI) to nontoxic trivalent chromium [Cr(III)] prior to systemic absorption. This study examines dose-related pharmacokinetics in humans following repeated oral exposure to Cr(VI) in drinking water. In particular, we sought to examine whether plausible drinking water exposures to Cr(VI) caused a sustained increase in red blood cell chromium levels, a specific marker for systemic uptake of Cr(VI). Adult male volunteers ingested a liter (in three volumes of 333 ml, at approximate 6-hr intervals) of deionized water containing Cr(VI) concentrations ranging from 0.1 to 10.0 mg/liter. Samples of urine, plasma, and red blood cells were collected and analyzed for chromium. A dose-related increase in urinary chromium excretion was observed in all volunteers. Red blood cell and plasma chromium concentrations became elevated in certain individuals at the highest doses. The RBC chromium profiles suggest that the ingested Cr(VI) was reduced to Cr(III) before entering the bloodstream, since the chromium concentration in the RBCs dropped rapidly postexposure. These findings suggest that the human gastrointestinal tract has the capacity to reduce ingested Cr(VI) following ingestion of up to 1 liter of water containing 10.0 mg/liter of Cr(VI), which is consistent with USEPA's position that the Cr(VI) drinking water standard of 0.10 mg Cr(VI)/liter is below the reductive capacity of the stomach.

Administration, Oral↗