Cardno ChemRisk

Chicago, IL, United States

Cardno ChemRisk

Chicago, IL, United States
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Perez A.L.,Cardno ChemRisk | Liong M.,Cardno ChemRisk | Plotkin K.,Cardno ChemRisk | Rickabaugh K.P.,RJ Lee Group, Inc | Paustenbach D.J.,Cardno ChemRisk
Chemosphere | Year: 2017

This study provides an exposure and risk assessment of diundecyl phthalate (DUP), a high molecular weight phthalate plasticizer present in automobile interiors. Total daily intake of DUP was calculated from DUP measured in wipe samples from vehicle seats from six automobiles. Four of the vehicles exhibited atypical visible surface residue on the seats. Two vehicles with no visible surface residue were sampled as a comparison. DUP was the predominant organic compound identified in each of the wipes from all seats. A risk assessment of DUP via oral, dermal, and inhalation routes resulting from contact with automobile seats was conducted. The mean, standard deviation, and maximum DUP concentrations on the seats with visible surface residue were 6983 ± 7823 μg/100 cm2 and 38300 μg/100 cm2, respectively. The mean and 95th percentile of the mean for daily cumulative dose of DUP for all exposure routes for the seats with no visible surface residue ranged from 7 × 10−4 to 4 × 10−3 mg/kg-day and from 8 × 10−4 to 5 × 10−3 mg/kg-day, respectively. For seats with visible surface residue, cumulative doses ranged from 2 × 10−3 to 2 × 10−2 mg/kg-day and from 4 × 10−3 to 2 × 10−2 mg/kg-day, respectively. The estimated daily intake (contact or absorbed dose) of DUP from automobile seats were far lower than the NOAELs reported in and derived from animal studies, and are well below the reported Registration, Evaluation, Authorisation and Restriction of Chemicals (REACH) Derived No Effect Levels (DNELs) for the general population. Based on this analysis, using virtually any benchmark for evaluating safety, exposure to DUP via automobile seat covers did not pose a measureable increased health-risk in any population under any reasonably plausible exposure scenario. © 2016 Elsevier Ltd

Barlow C.A.,Cardno ChemRisk | Sahmel J.,Cardno ChemRisk | Paustenbach D.J.,Carndo ChemRisk | Henshaw J.L.,Cardno ChemRisk
Critical Reviews in Toxicology | Year: 2017

The understanding by industrial hygienists of the hazards of asbestos and appropriate ways to characterize and control exposure has evolved over the years. Here, a detailed analysis of the evolution of industrial hygiene practices regarding asbestos and its health risks, from the early 1900s until the advent of the national occupational health and safety regulatory structure currently in place in the US (early-to-mid 1970s) is presented. While industrial hygienists recognized in the early 1900s that chronic and high-level exposures to airborne concentrations of asbestos could pose a serious health hazard, it was not until the mid-1950s that the carcinogenic nature of asbestos began to be characterized and widespread concern followed. With the introduction of the membrane filter sampling method in the late 1960s and early 1970s, asbestos sampling and exposure assessment capabilities advanced to a degree which allowed industrial hygienists to more precisely characterize the exposure–response relationship. The ability of industrial hygienists, analytical chemists, toxicologists, and physicians to more accurately define this relationship was instrumental to the scientific community’s ability to establish Occupational Exposure Levels (OELs) for asbestos. These early developments set the stage for decades of additional study on asbestos exposure potential and risk of disease. This was followed by the application of engineering controls and improved respiratory protection which, over the years, saved thousands of lives. This paper represents a state-of-the-art review of the knowledge of asbestos within the industrial hygiene community from about 1900 to 1975. © 2017 Informa UK Limited, trading as Taylor & Francis Group.

Pierce J.S.,Cardno ChemRisk | Ruestow P.S.,Cardno ChemRisk | Finley B.L.,Cardno ChemRisk
Critical Reviews in Toxicology | Year: 2016

Although consumption of chrysotile asbestos has decreased since the 1970s, the latency period of asbestos-related cancers is thought to be at least 20–30 years, and therefore the potential health risks associated with historical exposures is still actively researched. This analysis represents an update to a previous paper in which we evaluated the exposure–response relationships for lung cancer and mesothelioma in chrysotile-exposed cohorts. Here, we review several recently published studies as well as updated information from previous studies. For each of the 14 studies considered, we identified the “no-observed adverse effect level” (NOAEL) for lung cancer and/or mesothelioma. NOAEL values for lung cancer ranged from 1.1 to <20 f/cc-years to 1600–3200 f/cc-years, and for mesothelioma ranged from 100–400 f/cc-years to 800–1599 f/cc-years. The range of “best estimate” NOAELs was estimated to be 89–168 f/cc-years for lung cancer and 208–415 f/cc-years for mesothelioma. None of the six cohorts of cement or friction product manufacturing workers exhibited an increased lung cancer risk at any exposure level, while all of the five studies of textile workers reported an increased risk at one or more exposure levels. This is likely because friction and cement workers were exposed to much shorter chrysotile fibers. Of the seven cases of peritoneal mesothelioma reported in the included studies, none were observed in the analyses of cement or friction product manufacturing workers in the absence of crocidolite exposure. These findings will help characterize potential worker and consumer health risks associated with historical and current chrysotile exposures. © 2016 Informa UK Limited, trading as Taylor & Francis Group.

Paustenbach D.J.,Cardno ChemRisk | Galbraith D.A.,Cardno ChemRisk | Finley B.L.,Cardno ChemRisk
Clinical Toxicology | Year: 2014

Introduction. There has been some recent concern regarding possible systemic health effects resulting from elevated blood cobalt concentrations in patients with cobalt containing hip implants. To date there are no blood cobalt criteria to help guide physicians when evaluating an individual hip implant patient's risk of developing systemic health effects because historically there was little or no concern about systemic cobalt toxicity in implant patients. Objective. Our purpose is to describe recently completed research regarding the relationship between blood cobalt concentrations and clinical health effects. We discuss the possibility of systemic health effects in patients with metal containing implants and propose various blood cobalt concentrations that are not associated with an increased risk of developing certain adverse effects. Methodology. The primary literature search was conducted using PubMed and Web of Science using the following search terms: cobalt AND (toxicity OR health effects OR cardiotoxicity OR hematological OR endocrine OR immunological OR reproductive OR testicular effects OR neurological OR case report OR cohort OR Roncovite). The searches identified 6786 papers of which 122 were considered relevant. The Agency for Toxic Substances and Disease Registry toxicological profile for cobalt and the U.S. Environmental Protection Agency Office of Research and Development's National Center for Environmental Assessment's documentation on the provisional peer-reviewed toxicity value for cobalt were also utilized to identify secondary literature sources. Results. Our review of the toxicology and medical literature indicates that highly elevated blood cobalt concentrations can result in certain endocrine, hematological, cardiovascular, and neurological effects in animals and/or humans. These studies, in addition to historical clinical findings involving the therapeutic use of cobalt, indicate that significant systemic effects of cobalt will not occur below blood cobalt concentrations of 300 μg/L in most persons. Some individuals with specific risk factors for increased susceptibility (e.g., severe and sustained hypoalbuminemia) may exhibit systemic effects at lower cobalt blood concentrations. This review also describes several cobalt dosing studies performed with human volunteers that consumed cobalt for 15, 30, or 90 days. Overall, the results of these dosing studies indicate that sustained blood cobalt concentrations averaging 10-70 μg/L for up to 90 days cause no significant clinical effects (maximum concentrations approached 120 μg/L). Some proposed blood criteria for assessing implant wear and local tissue damage have been suggested by several medical groups. For example, the UK Medicines and Healthcare Products Regulatory Agency has proposed a blood cobalt guidance value of 7 μg/L, and the Mayo Clinic has suggested serum cobalt concentrations greater than 10 μg/L, but both of these values are primarily intended to address implant wear and to alert physicians to the possibility of an increased incidence of local effects. There is a clear lack of consensus regarding how to identify a specific numerical blood concentration of concern and whether whole blood or serum is a better matrix to assess total cobalt concentration. Conclusions. Based on currently available data, only under very unusual circumstances should a clinician expect that biologically important systemic adverse effects might occur in implant patients with blood cobalt concentrations less than 300 μg/L. Patients with metal-containing hip implants who exhibit signs or symptoms potentially related to polycythemia, hypothyroidism, neurological, or cardiac dysfunction should be clinically evaluated for these conditions. Polycythemia appears to be the most sensitive endpoint. © 2014 Informa Healthcare USA, Inc.

Unice K.M.,Cardno ChemRisk | Kerger B.D.,Cardno ChemRisk | Paustenbach D.J.,Cardno ChemRisk | Finley B.L.,Cardno ChemRisk | Tvermoes B.E.,Cardno ChemRisk
Chemico-Biological Interactions | Year: 2014

An updated biokinetic model for human exposures to cobalt (Co) was developed based on a comprehensive set of human pharmacokinetics data collected from five male and five female volunteers who ingested ∼1 mg Co/day of a Co supplement for 3 months. Three key experimental observations from the human dosing studies were incorporated into the model: (1) an increase in the measured fraction of large molecular serum protein bound Co from 95% during dosing to 99% after dosing; (2) a linear decrease in Co red blood cell concentration after dosing; and (3) Co renal clearance consistent with estimated glomerular filtration rates and free Co2+ concentration. The model was refined by adding compartments accounting for (1) albumin bound Co in intravascular fluid (serum); (2) albumin bound Co in extravascular fluid with physiologic exchange rates of albumin bound Co between extravascular and intravascular fluid; and (3) a novel sequential cascade of compartments representing red blood cell ages between 1 and 120 days. Reasonable agreement between the modeled and measured urine, serum, and whole blood concentrations were observed (r > 0.84, slope = 0.79-1.0) with gastrointestinal absorption rates between 9% and 66%. In addition, model predictions agreed well with data from several external studies representing healthy human volunteers, dialysis patients, anephric patients, a Co-poisoning incident and whole body retention studies. Our revised model considerably improves the state of knowledge on human Co kinetics, and should be helpful for evaluating elevated blood Co concentrations in currently exposed populations, such as metal-on-metal (MoM) hip implant patients. © 2014 Elsevier Ireland Ltd. All rights reserved.

Fedak K.M.,Colorado State University | Bernal A.,Cardno ChemRisk | Capshaw Z.A.,Cardno ChemRisk | Gross S.,Cardno ChemRisk
Emerging Themes in Epidemiology | Year: 2015

In 1965, Sir Austin Bradford Hill published nine "viewpoints" to help determine if observed epidemiologic associations are causal. Since then, the "Bradford Hill Criteria" have become the most frequently cited framework for causal inference in epidemiologic studies. However, when Hill published his causal guidelines - just 12 years after the double-helix model for DNA was first suggested and 25 years before the Human Genome Project began - disease causation was understood on a more elementary level than it is today. Advancements in genetics, molecular biology, toxicology, exposure science, and statistics have increased our analytical capabilities for exploring potential cause-and-effect relationships, and have resulted in a greater understanding of the complexity behind human disease onset and progression. These additional tools for causal inference necessitate a re-evaluation of how each Bradford Hill criterion should be interpreted when considering a variety of data types beyond classic epidemiology studies. Herein, we explore the implications of data integration on the interpretation and application of the criteria. Using examples of recently discovered exposure-response associations in human disease, we discuss novel ways by which researchers can apply and interpret the Bradford Hill criteria when considering data gathered using modern molecular techniques, such as epigenetics, biomarkers, mechanistic toxicology, and genotoxicology. © 2015 Fedak et al.

Cyrs W.D.,Cardno ChemRisk | Avens H.J.,Cardno ChemRisk | Capshaw Z.A.,Cardno ChemRisk | Kingsbury R.A.,Cardno ChemRisk | And 2 more authors.
Energy Policy | Year: 2014

Grid-connected solar photovoltaic (PV) power is currently one of the fastest growing power-generation technologies in the world. While PV technologies provide the environmental benefit of zero emissions during use, the use of heavy metals in thin-film PV cells raises important health and environmental concerns regarding the end-of-life disposal of PV panels. To date, there is no published quantitative assessment of the potential human health risk due to cadmium leaching from cadmium telluride (CdTe) PV panels disposed in a landfill. Thus, we used a screening-level risk assessment tool to estimate possible human health risk associated with disposal of CdTe panels into landfills. In addition, we conducted a literature review of potential cadmium release from the recycling process in order to contrast the potential health risks from PV panel disposal in landfills to those from PV panel recycling. Based on the results of our literature review, a meaningful risk comparison cannot be performed at this time. Based on the human health risk estimates generated for PV panel disposal, our assessment indicated that landfill disposal of CdTe panels does not pose a human health hazard at current production volumes, although our results pointed to the importance of CdTe PV panel end-of-life management. © 2014 Elsevier Ltd.

Pierce J.S.,Cardno ChemRisk | Abelmann A.,Cardno ChemRisk | Spicer L.J.,Cardno ChemRisk | Adams R.E.,Cardno ChemRisk | Finley B.L.,Cardno ChemRisk
Critical Reviews in Toxicology | Year: 2014

Diacetyl and 2,3-pentanedione inhalation have been suggested as causes of severe respiratory disease, including bronchiolitis obliterans, in food/flavoring manufacturing workers. Both compounds are present in many food items, tobacco, and other consumer products, but estimates of exposures associated with the use of these goods are scant. A study was conducted to characterize exposures to diacetyl and 2,3-pentanedione associated with cigarette smoking. The yields (μg/cigarette) of diacetyl and 2,3-pentanedione in mainstream (MS) cigarette smoke were evaluated for six tobacco products under three smoking regimens (ISO, Massachusetts Department of Public Health, and Health Canada Intense) using a standard smoking machine. Mean diacetyl concentrations in MS smoke ranged from 250 to 361 ppm for all tobacco products and smoking regimens, and mean cumulative exposures associated with 1 pack-year ranged from 1.1 to 1.9 ppm-years. Mean 2,3-pentanedione concentrations in MS smoke ranged from 32.2 to 50.1 ppm, and mean cumulative exposures associated with 1 pack-year ranged from 0.14 to 0.26 ppm-years. We found that diacetyl and 2,3-pentanedione exposures from cigarette smoking far exceed occupational exposures for most food/flavoring workers who smoke. This suggests that previous claims of a significant exposure-response relationship between diacetyl inhalation and respiratory disease in food/flavoring workers were confounded, because none of the investigations considered or quantified the non-occupational diacetyl exposure from cigarette smoke, yet all of the cohorts evaluated had considerable smoking histories. Further, because smoking has not been shown to be a risk factor for bronchiolitis obliterans, our findings are inconsistent with claims that diacetyl and/or 2,3-pentanedione exposure are risk factors for this disease. © 2014 Informa Healthcare USA, Inc.

Dahlen E.,Cardno ChemRisk
Journal of Environmental Hydrology | Year: 2013

While promising to make huge quantities of oil and gas available from already existing shale reservoirs, hydraulic fracturing produces very high volumes of saline water as a by-product. What questions should operators be asking to address economic risk caused by varying formation geochemistry, regulatory uncertainty, and the complexity of wastewater treatment options? © 2013 International Association for Environmental Hydrology.

Sahmel J.,Cardno ChemRisk
Journal of Exposure Science and Environmental Epidemiology | Year: 2015

The potential for para-occupational, domestic, or take-home exposures from asbestos-contaminated work clothing has been acknowledged for decades, but historically has not been quantitatively well characterized. A simulation study was performed to measure airborne chrysotile concentrations associated with laundering of contaminated clothing worn during a full shift work day. Work clothing fitted onto mannequins was exposed for 6.5 h to an airborne concentration of 11.4 f/cc (PCME) of chrysotile asbestos, and was subsequently handled and shaken. Mean 5-min and 15-min concentrations during active clothes handling and shake-out were 3.2 f/cc and 2.9 f/cc, respectively (PCME). Mean airborne PCME concentrations decreased by 55% 15 min after clothes handling ceased, and by 85% after 30 min. PCM concentrations during clothes handling were 11–47% greater than PCME concentrations. Consistent with previously published data, daily mean 8-h TWA airborne concentrations for clothes-handling activity were approximately 1.0% of workplace concentrations. Similarly, weekly 40-h TWAs for clothes handling were approximately 0.20% of workplace concentrations. Estimated take-home cumulative exposure estimates for weekly clothes handling over 25-year working durations were below 1 f/cc-year for handling work clothes contaminated in an occupational environment with full shift airborne chrysotile concentrations of up to 9 f/cc (8-h TWA).Journal of Exposure Science and Environmental Epidemiology advance online publication, 29 April 2015; doi:10.1038/jes.2015.15. © 2015 Nature America, Inc.

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