Joyce S Tsuji

University of Arkansas at Little Rock, Little Rock, AR, United States

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Publications (19)52.48 Total impact

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    ABSTRACT: While exposures to high levels of arsenic in drinking water are associated with excess cancer risk (e.g., skin, bladder, and lung), exposures at lower levels (e.g., <100-200μg/L) generally are not. Lack of significant associations may result from methodological issues (e.g., inadequate statistical power, exposure misclassification), or a different dose-response relationship at low exposures, possibly associated with a toxicological mode of action that requires a sufficient dose for increased tumor formation. The extent to which bladder cancer risk for low-level arsenic exposure can be statistically measured by epidemiological studies was examined using an updated meta-analysis of bladder cancer risk with data from two new publications. The summary relative risk estimate (SRRE) for all nine studies was elevated slightly, but not significantly (1.07; 95% confidence interval [CI]: 0.95-1.21, p-Heterogeneity [p-H]=0.543). The SRRE among never smokers was 0.85 (95% CI: 0.66-1.08, p-H=0.915), whereas the SRRE was positive and more heterogeneous among ever smokers (1.18; 95% CI: 0.97-1.44, p-H=0.034). The SRRE was statistically significantly lower than relative risks predicted for never smokers in the United States based on linear extrapolation of risks from higher doses in southwest Taiwan to arsenic water exposures >10μg/L for more than one-third of a lifetime. By contrast, for all study subjects, relative risks predicted for one-half of lifetime exposure to 50μg/L were just above the upper 95% CI on the SRRE. Thus, results from low-exposure studies, particularly for never smokers, were statistically inconsistent with predicted risk based on high-dose extrapolation. Additional studies that better characterize tobacco use and stratify analyses of arsenic and bladder cancer by smoking status are necessary to further examine risks of arsenic exposure for smokers.
    Toxicology 01/2014; · 4.02 Impact Factor
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    ABSTRACT: The recent EPA Framework for Metals Risk Assessment provides the opportunity for contextual risk assessment for sites impacted by metals (such as the depicted Dauntless Mine in Colorado).
    Environmental Science and Technology 11/2009; 43(22):8478-82. · 5.26 Impact Factor
  • 08/2009: pages 543 - 580; , ISBN: 9780470747803
  • Joyce S Tsuji, Michael R Garry
    Risk Analysis 01/2009; 29(4):490-1; discussion 492-7. · 2.28 Impact Factor
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    ABSTRACT: Although exposure to high levels of arsenic in drinking water is associated with excess cancer risk (e.g., skin, bladder, and lung), lower exposures (e.g., <100-200 microg/L) generally are not. Lack of significant associations at lower exposures may be attributed to methodologic issues (e.g., inadequate statistical power, exposure misclassification), or to differences in the dose-response relationship at high versus low exposures. The objectives of this review and meta-analysis were to evaluate associations, examine heterogeneity across studies, address study design and sample size issues, and improve the precision of estimates. Eight studies of bladder cancer and low-level arsenic exposure met our inclusion criteria. Meta-analyses of never smokers produced summary relative risk estimates (SRREs) below 1.0 (highest versus lowest exposure). The SRRE for never and ever smokers combined was elevated slightly, but not significantly (1.11; 95% CI: 0.95-1.30). The SRRE was somewhat elevated among ever smokers (1.24; 95% CI: 0.99-1.56), and statistical significance was observed in some subgroup analyses; however, heterogeneity across studies was commonly present. Although uncertainties remain, low-level arsenic exposure alone did not appear to be a significant independent risk factor for bladder cancer. More studies with detailed smoking history will help resolve whether smoking is an effect modifier.
    Regulatory Toxicology and Pharmacology 09/2008; 52(3):299-310. · 2.13 Impact Factor
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    ABSTRACT: Background exposures provide perspective for interpreting calculated health risks associated with naturally occurring substances such as arsenic. Background inorganic arsenic intake from diet and water for children (ages 1-6 years) and all ages of the U.S. population was modeled stochastically using consumption data from USDA, published data on inorganic arsenic in foods, and EPA data on arsenic in drinking water. Mean and 90th percentile intakes for the U.S. population were 5.6 and 10.5 microg/day, assuming nationwide compliance with the 10 microg/L U.S. drinking water standard. Intakes for children were slightly lower (3.5 and 5.9 microg/day). Based on the current EPA cancer slope factor for arsenic, estimated lifetime risks associated with background diet and water at the mean and 90th percentile are 1 per 10,000 and 2 per 10,000, respectively. By comparison, reasonable maximum risks for arsenic in soil at 20 (higher typical background level) and 100mg/kg are 4 per 100,000 and 2 per 10,000, using EPA default exposure assumptions. EPA reasonable maximum estimates of arsenic exposure from residential use of treated wood are likewise within background intakes. These examples provide context on how predicted risks compare to typical exposures within the U.S. population, thereby providing perspective for risk communication and regulatory decision-making on arsenic in the environment and in consumer products.
    Regulatory Toxicology and Pharmacology 07/2007; 48(1):59-68. · 2.13 Impact Factor
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    ABSTRACT: Lumber treated with chromated copper arsenate (CCA) compounds has been used in residential outdoor wood structures and public playgrounds. The U.S. Environmental Protection Agency (EPA) has conducted a probabilistic assessment of children's exposure to arsenic using the Stochastic Human Exposure and Dose Simulation model for the wood preservative scenario (SHEDS-Wood). The assessment relied on data derived from an experimental study conducted using adult volunteers and designed to result in maximum hand and wipe loadings to estimate the residue-skin transfer efficiency. Recent analyses of arsenic hand-loading data generated by studies of children actively involved in playing on CCA-treated structures indicate that the transfer efficiency coefficient and hand-loading estimates derived from the experimental study significantly overestimate the amount that occurs during actual play. Our goal was to assess the feasibility of using child hand-loading data in the SHEDS-Wood model and their impact on exposure estimates. We used data generated by the larger of the studies of children in SHEDS-Wood, instead of the distributions used by U.S. EPA. We compared our estimates of the lifetime average daily dose (LADD) and average daily dose (ADD) with those derived by the U.S. EPA. Our analysis indicates that data from observational studies of children can be used in SHEDS-Wood. Our estimates of the mean (and 95th percentile) LADD and ADD were 27% (10%) and 29% (15%) of the estimates derived by U.S. EPA. We recommend that the SHEDS-Woods model use data from studies of children actively playing on playsets to more accurately estimate children's actual exposures to CCA.
    Environmental Health Perspectives 06/2007; 115(5):781-6. · 7.26 Impact Factor
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    Leila M Barraj, Joyce S Tsuji
    Risk Analysis 03/2007; 27(1):1-3; author reply 5-6. · 2.28 Impact Factor
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    ABSTRACT: Engineered nano-scale materials are increasingly being used in a variety of consumer products. Health risk assessments are critical to evaluate the potential hazards associated with release of these materials and to ensure regulatory and public acceptance. Exposure and toxicity comprise the main components of risk. Materials science evaluations of nano-engineered particle exposures during production and throughout product lifetime may involve relatively simple tribology and reliability testing, and long-term stability assessment. Even without testing, existing knowledge of the properties of resins and binders can be used to formulate durable products that retain nanomaterials. Standard screening tests for toxicity are currently under development. Research has focused on some of the most common types of nanomaterials in or destined for products. A wealth of related information is also available from ultrafine particles (UFPs), metal fumes, volatile organic compounds, and mineral fibers. The presented approach describes the interplay between exposure, materials science, and toxicity, which when taken together, can aid in characterizing risk of products, engineering "safety" in products containing nanomaterials.
    01/2007;
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    ABSTRACT: Nanoparticles are small-scale substances (<100 nm) with unique properties and, thus, complex exposure and health risk implications. This symposium review summarizes recent findings in exposure and toxicity of nanoparticles and their application for assessing human health risks. Characterization of airborne particles indicates that exposures will depend on particle behavior (e.g., disperse or aggregate) and that accurate, portable, and cost-effective measurement techniques are essential for understanding exposure. Under many conditions, dermal penetration of nanoparticles may be limited for consumer products such as sunscreens, although additional studies are needed on potential photooxidation products, experimental methods, and the effect of skin condition on penetration. Carbon nanotubes apparently have greater pulmonary toxicity (inflammation, granuloma) in mice than fine-scale carbon graphite, and their metal content may affect toxicity. Studies on TiO2 and quartz illustrate the complex relationship between toxicity and particle characteristics, including surface coatings, which make generalizations (e.g., smaller particles are always more toxic) incorrect for some substances. These recent toxicity and exposure data, combined with therapeutic and other related literature, are beginning to shape risk assessments that will be used to regulate the use of nanomaterials in consumer products.
    Toxicological Sciences 01/2006; 89(1):42-50. · 4.33 Impact Factor
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    ABSTRACT: In response to concerns regarding arsenic in soil from a pesticide manufacturing plant, we conducted a biomonitoring study on children younger than 7 years of age, the age category of children most exposed to soil. Urine samples from 77 children (47% participation rate) were analyzed for total arsenic and arsenic species related to ingestion of inorganic arsenic. Older individuals also provided urine (n = 362) and toenail (n = 67) samples. Speciated urinary arsenic levels were similar between children (geometric mean, geometric SD, and range: 4.0, 2.2, and 0.89-17.7 microg/L, respectively) and older participants (3.8, 1.9, 0.91-19.9 microg/L) and consistent with unexposed populations. Toenail samples were < 1 mg/kg. Correlations between speciated urinary arsenic and arsenic in soil (r = 0.137, p = 0.39; n = 41) or house dust (r = 0.049, p = 0.73; n = 52) were not significant for children. Similarly, questionnaire responses indicating soil exposure were not associated with increased urinary arsenic levels. Relatively low soil arsenic exposure likely precluded quantification of arsenic exposure above background.
    Environmental Health Perspectives 12/2005; 113(12):1735-40. · 7.26 Impact Factor
  • Regulatory Toxicology and Pharmacology 12/2004; 40(3):372. · 2.13 Impact Factor
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    ABSTRACT: Health risks to children from chemicals in soil and consumer products have become a regulatory focus in the U.S. This study reviews short-term health effect levels for arsenic exposure in young children (i.e., 0-6 years old). Acute health effects are described mostly in adults in case reports of arsenic poisoning from water or food and in studies of medicinal arsenic treatment. Several epidemiological studies report health effects from subchronic arsenic exposure in children primarily from drinking water in developing countries. Acute health effects typically include gastrointestinal, neurological, and skin effects, and in a few cases facial edema and cardiac arrhythmia. Dermatoses are most consistently reported in both adults and children with subchronic exposure. With low exposure, the prevalence and severity of disease generally increases with age (i.e., length of exposure) and arsenic dose. The available data collectively indicate a lowest-observed-adverse-effect level around 0.05mg/kg-day for both acute and subchronic exposure. At low doses, children do not appear to be more sensitive than adults on a dose-per-body-weight basis, although data for acute exposures are limited and uncertainties exist for quantifying potential neurological or vascular effects at low-level subchronic exposures. Based on these data, possible reference levels for acute and subchronic exposure in young children are 0.015 and 0.005mg/kg-day, respectively.
    Regulatory Toxicology and Pharmacology 05/2004; 39(2):99-110. · 2.13 Impact Factor
  • Regulatory Toxicology and Pharmacology - REGUL TOXICOL PHARMACOL. 01/2004; 40(3):374-375.
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    ABSTRACT: Arsenic is a natural component of the environment and is ubiquitous in soils, water, and the diet. Because dietary intake can be a significant source of background exposure to inorganic arsenic (the most toxicologically significant form), accurate intake estimates are needed to provide a context for risk management of arsenic exposure. Intake of inorganic arsenic by adults is fairly well characterized, but previous estimates of childhood intake were based on inorganic arsenic analyses in a limited number of foods (13 food types). This article estimates dietary intake for U.S. children (1 to 6 years of age) based on reported inorganic arsenic concentrations in 38 foods and in water used in cooking those foods (inorganic arsenic concentration of 0.8 μg/L), and U.S. Department of Agriculture food consumption data. This information is combined using a probabilistic software model to extract food consumption patterns and compute exposure distributions. The mean childhood dietary intake estimate for inorganic arsenic was 3.2 μg/day with a range of 1.6 to 6.2 μg/day for the 10th and 95th percentiles, respectively. For both the mean and 95th percentile inorganic arsenic intake rates, intake was predominantly contributed by grain and grain products, fruits and fruit juices, rice and rice products, and milk.
    Human and Ecological Risk Assessment - HUM ECOL RISK ASSESSMENT. 01/2004; 10(3):473-483.
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    ABSTRACT: We conducted a pooled analysis to investigate the relationship between exposure to elemental mercury in air and resulting urinary mercury levels, specifically at lower air levels relevant for environmental exposures and public health goals (i.e., < 50 microg/m3 down to 1.0 microg/m3). Ten studies reporting paired air and urine mercury data (149 samples total) met criteria for data quality and sufficiency. The log-transformed data set showed a strong correlation between mercury in air and in urine (r = 0.774), although the relationship was best fit by a series of parallel lines with different intercepts for each study R2 = 0.807). Predicted ratios of air to urine mercury levels at 50 microg/m3 air concentration ranged from 1:1 to 1:3, based on the regression line for the studies. Toward the lower end of the data set (i.e., 10 microg/m3), predicted urinary mercury levels encompassed two distinct ranges: values on the order of 20 microg/L and 30-60 microg/L. Extrapolation to 1 microg/m3 resulted in predicted urinary levels of 4-5 and 6-13 microg/L. Higher predicted levels were associated with use of static area air samplers by some studies rather than more accurate personal air samplers. Urinary mercury predictions based primarily on personal air samplers at 1 and 10 microg/m3 are consistent with reported mean (4 microg/L) and upper-bound (20 microg/L) background levels, respectively. Thus, although mercury levels in air and urine are correlated below 50 microg/m3, the impact of airborne mercury levels below 10 microg/m3 is likely to be indistinguishable from background urinary mercury levels.
    Environmental Health Perspectives 04/2003; 111(4):623-30. · 7.26 Impact Factor
  • Joyce S Tsuji, Sue Robinson
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    ABSTRACT: Risk assessment methods of developed countries have prescribed exposure assumptions for calculating health risks that are generally inappropriate for developing countries because of population, cultural, and social differences. For example, populations in developing countries are often subsistence users of natural resources with a more outdoor-oriented lifestyle. Assessments should thus measure specific dietary intake rates and contact rates with environmental media. Chemical analyses of food, environmental media, and any biomarkers of exposure should include a carefully matched reference population to distinguish between exposures due to naturally occurring metals in more mineralized areas and potential anthropogenic sources. Without a reference group, one might predict excess risk associated with the external source, even though exposure is due to background levels. For example, subsistence populations often have a simple diet with high ingestion rates of a few food types (e.g. 200 g/day wet weight of fish; 500 g/day of rice). These foods can be naturally elevated in arsenic (fish and rice) and mercury (fish). Conservative risk assessments that extrapolate toxicity from high to low doses can predict elevated risks for these naturally occurring elements (e.g. greater than 1 in 10,000 cancer risk for arsenic). Whether the calculated risks are actually indicative of harm to subsistence populations should be considered in light of the beneficial properties of the diet and the lack of alternative food choices.
    Toxicology 01/2003; 181-182:467-70. · 4.02 Impact Factor
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Publication Stats

279 Citations
8 Downloads
555 Views
52.48 Total Impact Points

Institutions

  • 2009
    • University of Arkansas at Little Rock
      • Department of Applied Sciences
      Little Rock, AR, United States
  • 2003–2009
    • Exponent
      San Mateo, California, United States