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Dive into the research topics where Helen Schurz Rogers is active.

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Featured researches published by Helen Schurz Rogers.


Environmental Health Perspectives | 2005

Case-control study of an acute aflatoxicosis outbreak, Kenya, 2004

Eduardo Azziz-Baumgartner; Kimberly Lindblade; Karen Gieseker; Helen Schurz Rogers; Stephanie Kieszak; Henry Njapau; Rosemary L. Schleicher; Leslie F. McCoy; Ambrose Misore; Kevin M. DeCock; Carol Rubin; Laurence Slutsker

Objectives: During January–June 2004, an aflatoxicosis outbreak in eastern Kenya resulted in 317 cases and 125 deaths. We conducted a case–control study to identify risk factors for contamination of implicated maize and, for the first time, quantitated biomarkers associated with acute aflatoxicosis. Design: We administered questionnaires regarding maize storage and consumption and obtained maize and blood samples from participants. Participants: We recruited 40 case-patients with aflatoxicosis and 80 randomly selected controls to participate in this study. Evaluations/Measurements: We analyzed maize for total aflatoxins and serum for aflatoxin B1–lysine albumin adducts and hepatitis B surface antigen. We used regression and survival analyses to explore the relationship between aflatoxins, maize consumption, hepatitis B surface antigen, and case status. Results: Homegrown (not commercial) maize kernels from case households had higher concentrations of aflatoxins than did kernels from control households [geometric mean (GM) = 354.53 ppb vs. 44.14 ppb; p = 0.04]. Serum adduct concentrations were associated with time from jaundice to death [adjusted hazard ratio = 1.3; 95% confidence interval (CI), 1.04–1.6]. Case patients had positive hepatitis B titers [odds ratio (OR) = 9.8; 95% CI, 1.5–63.1] more often than controls. Case patients stored wet maize (OR = 3.5; 95% CI, 1.2–10.3) inside their homes (OR = 12.0; 95% CI, 1.5–95.7) rather than in granaries more often than did controls. Conclusion: Aflatoxin concentrations in maize, serum aflatoxin B1–lysine adduct concentrations, and positive hepatitis B surface antigen titers were all associated with case status. Relevance: The novel methods and risk factors described may help health officials prevent future outbreaks of aflatoxicosis.


Cancer Epidemiology, Biomarkers & Prevention | 2008

Human Aflatoxin Albumin Adducts Quantitatively Compared by ELISA, HPLC with Fluorescence Detection, and HPLC with Isotope Dilution Mass Spectrometry

Leslie F. McCoy; Peter F. Scholl; Anne E. Sutcliffe; Stephanie Kieszak; Carissa D. Powers; Helen Schurz Rogers; Yun Yun Gong; John D. Groopman; Christopher P. Wild; Rosemary L. Schleicher

Essential to the conduct of epidemiologic studies examining aflatoxin exposure and the risk of heptocellular carcinoma, impaired growth, and acute toxicity has been the development of quantitative biomarkers of exposure to aflatoxins, particularly aflatoxin B1. In this study, identical serum sample sets were analyzed for aflatoxin-albumin adducts by ELISA, high-performance liquid chromatography (HPLC) with fluorescence detection (HPLC-f), and HPLC with isotope dilution mass spectrometry (IDMS). The human samples analyzed were from an acute aflatoxicosis outbreak in Kenya in 2004 (n = 102) and the measured values ranged from 0.018 to 67.0, nondetectable to 13.6, and 0.002 to 17.7 ng/mg albumin for the respective methods. The Deming regression slopes for the HPLC-f and ELISA concentrations as a function of the IDMS concentrations were 0.71 (r2 = 0.95) and 3.3 (r2 = 0.96), respectively. When the samples were classified as cases or controls, based on clinical diagnosis, all methods were predictive of outcome (P < 0.01). Further, to evaluate assay precision, duplicate samples were prepared at three levels by dilution of an exposed human sample and were analyzed on three separate days. Excluding one assay value by ELISA and one assay by HPLC-f, the overall relative SD were 8.7%, 10.5%, and 9.4% for IDMS, HPLC-f, and ELISA, respectively. IDMS was the most sensitive technique and HPLC-f was the least sensitive method. Overall, this study shows an excellent correlation between three independent methodologies conducted in different laboratories and supports the validation of these technologies for assessment of human exposure to this environmental toxin and carcinogen. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1653–7)


Environmental Health Perspectives | 2009

A Review of Events That Expose Children to Elemental Mercury in the United States

Robin Lee; Dan Middleton; Kathleen L. Caldwell; Steve M Dearwent; Steven K. Jones; Brian Lewis; Carolyn Monteilh; Mary E. Mortensen; Richard Nickle; Kenneth Orloff; Meghan Reger; John F. Risher; Helen Schurz Rogers; Michelle Watters

Objective Concern for children exposed to elemental mercury prompted the Agency for Toxic Substances and Disease Registry and the Centers for Disease Control and Prevention to review the sources of elemental mercury exposures in children, describe the location and proportion of children affected, and make recommendations on how to prevent these exposures. In this review, we excluded mercury exposures from coal-burning facilities, dental amalgams, fish consumption, medical waste incinerators, or thimerosal-containing vaccines. Data sources We reviewed federal, state, and regional programs with information on mercury releases along with published reports of children exposed to elemental mercury in the United States. We selected all mercury-related events that were documented to expose (or potentially expose) children. We then explored event characteristics (i.e., the exposure source, location). Data synthesis Primary exposure locations were at home, at school, and at other locations such as industrial property not adequately remediated or medical facilities. Exposure to small spills from broken thermometers was the most common scenario; however, reports of such exposures are declining. Discussion and conclusions Childhood exposures to elemental mercury often result from inappropriate handling or cleanup of spilled mercury. The information reviewed suggests that most releases do not lead to demonstrable harm if the exposure period is short and the mercury is properly cleaned up. Recommendations Primary prevention should include health education and policy initiatives. For larger spills, better coordination among existing surveillance systems would assist in understanding the risk factors and in developing effective prevention efforts.


Ciencia & Saude Coletiva | 2010

A review of events that expose children to elemental mercury in the United States

Robin Lee; Dan Middleton; Kathleen L. Caldwell; Steve M. Dearwent; Steven Jones; Brian Lewis; Carolyn Monteilh; Mary E. Mortensen; Richard Nickle; Kenneth Orloff; Meghan Reger; John F Risher; Helen Schurz Rogers; Michelle Watters

Concern for children exposed to elemental mercury prompted the Agency for Toxic Substances and Disease Registry and the Centers for Disease Control and Prevention to review the sources of elemental mercury exposures in children, describe the location and proportion of children affected, and make recommendations on how to prevent these exposures. In this review, we excluded mercury exposures from coal-burning facilities, dental amalgams, fish consumption, medical waste incinerators, or thimerosal-containing vaccines. We reviewed federal, state, and regional programs with data on mercury releases along with published reports of children exposed to elemental mercury in the United States. We selected all mercury-related events that were documented to expose (or potentially expose) children. Primary exposure locations were at home, at school, and at others such as industrial property not adequately remediated or medical facilities. Exposure to small spills from broken thermometers was the most common scenario; however, reports of such exposures are declining. The information reviewed suggests that most releases do not lead to demonstrable harm if the exposure period is short and the mercury is properly cleaned up. Primary prevention should include health education and policy initiatives.


BMC Research Notes | 2015

Paralytic shellfish poisonings resulting from an algal bloom in Nicaragua

Luis Callejas; Ana Cristian Melendez Darce; Juan José López Amador; Laura Conklin; Nicholas H. Gaffga; Helen Schurz Rogers; Stacey L. DeGrasse; Sherwood Hall; Marie C. Earley; Joanne Mei; Carol Rubin; Sylvain Aldighieri; Lorraine C. Backer; Eduardo Azziz-Baumgartner

BackgroundDuring an October 2005 algal bloom (i.e., a rapid increase or accumulation in the population of algae) off the coast of Nicaragua, 45 people developed symptoms of paralytic shellfish poisoning (PSP) and one person died. PSP in humans is caused by ingestion of saxitoxin, which is a neurotoxin often associated with shellfish contaminated by algal blooms.To explore the relationship between the algal bloom and human illnesses, we performed a case-control study of residents living in a coastal island. We administered a standardized clinical questionnaire, sampled locally harvested seafood and algae, and obtained urine samples for saxitoxin testing from symptomatic and asymptomatic persons. PSP case-patients were defined as island residents who developed at least one neurological symptom during the November 4–16 intoxication period. Seafood and algal samples were analyzed for saxitoxins using the receptor-binding assay and high-performance liquid chromatography. Two urine samples were analyzed for saxitoxins using a newly developed immunoassay.FindingsThree shellfish and two algal samples tested positive for saxitoxins. Ten (9%) of 107 participants developed neurological symptoms during the specified time period and five required hospitalization. While 6 (67%) of 9 possible case-patients and 21 (21%) of 98 controls had eaten fish (p=0.008), all case-patients and 17 (17%) of controls had eaten clams (P<0.0001). The saxitoxin concentration in the urine of a hospitalized case-patient was 21 ng saxitoxin/g creatinine compared to 0.16 ng saxitoxin/g creatinine in the single control patient’s urine.ConclusionsThese findings suggest that a bloom of saxitoxin-producing algae resulted in saxitoxin accumulation in local clams and was responsible for the PSP intoxication.


Clinical Toxicology | 2007

Exposure assessment of young children living in Chicago communities with historic reports of ritualistic use of mercury.

Helen Schurz Rogers; Joel Emery McCullough; Stephanie Kieszak; Kathleen L. Caldwell; Robert L. Jones; Carol Rubin

Objective. According to a 1997 finding, mercury was available for sale in several Chicago communities for use in spiritual or medicinal practice. Mercury used this way may impact the health of children. The Chicago Department of Public Health (CDPH) and the Centers for Disease Control and Prevention conducted a study to 1) quantify mercury exposure in biological specimens collected from a pediatric clinic or home visit in selected neighborhoods in Chicago, and 2) investigate possible sources of mercury exposure in homes. Methods. An exposure assessment study design was chosen to determine whether children living in Chicago communities that historically sold mercury were exposed to mercury vapor. We enrolled and collected biological samples from 306 children aged 2–10 years. In addition, we enrolled 42 children during a door-to-door survey of community residents. All the urine samples were analyzed for elemental or inorganic mercury. We also analyzed 43 blood samples to assess dietary mercury. Results. Overall geometric mean urine mercury was 0.26μg/L. Urine mercury levels did not differ among the three clinics or between the various participant groups. We did not find any association between ritualistic mercury use and exposure to mercury. Conclusions. Although pediatric mercury exposure does not appear to be problematic among our study population, mercury remains a potential health threat as long as it is readily available in communities. Healthcare providers should be aware of the potential for mercury exposure. Physicians and patients may call the National Poison Control Centers (1-800-222-1222) for information about diagnosis, testing, and treatment for all types of exposures, including exposure to mercury. Professionals are available 24 hours a day.


Military Medicine | 2006

Strategies for recognizing acute chemical-associated foodborne illness

Joshua G. Schier; Helen Schurz Rogers; Manish M. Patel; Carol A. Rubin; Martin Belson

The U.S. food supply is vulnerable to contamination with chemicals and toxins. Public health officials and clinicians may misdiagnose patients with acute chemical-associated foodborne illness (CAFI) due to unfamiliarity with chemical illness, increased familiarity with infectious foodborne illness, nonspecific presentation of most foodborne chemical poisoning, lack of readily available analytic methodologies to detect chemicals, and lack of education on how to develop a differential diagnosis for CAFI. This article will review the unique features of CAFI in the acute setting, address important questions to help differentiate CAFI from other foodborne illness, discuss laboratory features of CAFI, and provide health officials and clinicians with a clinical symptom-based approach to assist with proper identification and differentiation of acute CAFI.


Environmental Health Perspectives | 2006

Workgroup Report: Public Health Strategies for Reducing Aflatoxin Exposure in Developing Countries

Heather Strosnider; Eduardo Azziz-Baumgartner; Marianne Bänziger; Ramesh V. Bhat; Robert E Breiman; Marie-Noel Brune; Kevin M. DeCock; Abby Dilley; John D. Groopman; Kerstin Hell; Sara H. Henry; Daniel P. Jeffers; Curtis M. Jolly; Pauline E. Jolly; Gilbert N. Kibata; Lauren Lewis; Xiumei Liu; George Luber; Leslie F. McCoy; Patience Mensah; Marina Miraglia; Ambrose Misore; Henry Njapau; Choon Nam Ong; Mary T.K. Onsongo; Samuel W. Page; Douglas L. Park; Manish Patel; Timothy D. Phillips; Maya Pineiro


Morbidity and Mortality Weekly Report | 2016

Blood Lead Levels Among Children Aged <6 Years - Flint, Michigan, 2013-2016.

Chinaro Kennedy; Ellen E. Yard; Timothy Dignam; Sharunda Buchanan; Suzanne Condon; Mary Jean Brown; Jaime Raymond; Helen Schurz Rogers; John Sarisky; Rey de Castro; Ileana Arias; Patrick Breysse


Journal of Urban Health-bulletin of The New York Academy of Medicine | 2008

Mercury Exposure in Young Children Living in New York City

Helen Schurz Rogers; Nancy Jeffery; Stephanie Kieszak; Pat Fritz; Henry M. Spliethoff; Christopher D. Palmer; Patrick J. Parsons; Daniel Kass; Kathy Caldwell; George Eadon; Carol Rubin

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Carol Rubin

Centers for Disease Control and Prevention

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Kathleen L. Caldwell

Centers for Disease Control and Prevention

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Lorraine C. Backer

Centers for Disease Control and Prevention

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Stephanie Kieszak

Centers for Disease Control and Prevention

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Brian Lewis

Centers for Disease Control and Prevention

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Eduardo Azziz-Baumgartner

Centers for Disease Control and Prevention

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Leslie F. McCoy

Centers for Disease Control and Prevention

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Mary E. Mortensen

Centers for Disease Control and Prevention

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Henry M. Spliethoff

New York State Department of Health

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Henry Njapau

Food and Drug Administration

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