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Biomedical subjects

J R Reigart

Publications and source records attributed to J R Reigart.

At least 19 recordsLinked to original sources
PubMed2001

Pesticides in children.

Children are exposed to a wide range of pesticides, including insecticides, herbicides, fungicides, and rodenticides. They differ from adults in their exposures and responses to exposures. Acute and chronic toxicity are discussed, and important chronic effects, such as carcinogenesis, endocrine disruption, and neurodevelopment effects are reviewed. The state of laws and regulations are also discussed. Recommendations are made to pediatricians regarding treatment and advising families regarding avoidance of pesticide exposures and their effects.

Child↗
PubMed2001

Time required for blood lead levels to decline in nonchelated children.

OBJECTIVE: To determine the time for a decline in blood lead to less than 10 microg/dL in nonchelated children who are enrolled in case management. STUDY DESIGN: Retrospective analysis of venous blood lead data of lead-poisoned children followed in a case management program designed to decrease lead exposure. Children were excluded if their blood lead had not yet declined to less than 10 microg/dL, if they received chelation therapy, or if they had not received follow-up for more than 15 months. We calculated the time between peak elevation of lead and decline to less than 10 microg/dL. Data were categorized based on the child's peak blood lead and season in which their peak blood lead occurred. Data were analyzed using ANOVA and linear regression. Kaplan-Meier survival analysis was used to describe data in population form. RESULTS: 579 patients were included in the analysis. Blood leads of 25-29, 20-24, 15-19, and 10-14 microg/dL required 24.0, 20.9, 14.3, and 9.2 months, respectively, to decline to less than 10 microg/dL. For continuous data, a linear relationship was described by the following equation: Time (# of months required to achieve a blood lead less than 10 microg/dL) = 0.845 x peak lead; p < 0.0001. Kaplan-Meier curves complement the findings in a population-based fashion. CONCLUSIONS: The mean time for blood lead to decline was linearly related to the peak in blood lead. The time for 50% of the blood lead to decline to less than 10 microg/dL was not linear and varied with peak lead.

Chelation Therapy↗
PubMed2001

When do medical students identify career-influencing physician role models?

PURPOSE: To identify when medical students gain physician role models relative to when they make their specialty choices. METHOD: The 1998 graduating class of one medical school was surveyed about when and where they had made contact with their role models and whether they had made contact before or after making their specialty choices. Students also provided data about their demographics, curriculum pathways (problem-based or traditional), and specialty choices at matriculation and graduation. RESULTS: Of the 89 graduating seniors who responded (62%), 21 had role models they had known prior to matriculation, 51 had encountered their role models in medical school, and 51 had met their role models before making their specialty choices. Of the 51 students who had encountered their role models in medical school, 33 (65%) had done so before making their specialty choices. The mean time from matriculation to meeting a role model was 24.9 +/- 11.6 months, and students on the problem-based learning pathway had met their role models earlier than had students on the traditional pathway. CONCLUSIONS: Most medical students have physician role models at graduation, and many of these students identify their physician role models at a point when the interactions can influence their specialty choices.

Adult↗
PubMed1998

Children's health and the environment: a new agenda for prevention research.

Patterns of illness in American children have changed dramatically in this century. The ancient infectious diseases have largely been controlled. The major diseases confronting children now are chronic and disabling conditions termed the "new pediatric morbidity"--asthma mortality has doubled; leukemia and brain cancer have increased in incidence; neurodevelopmental dysfunction is widespread; hypospadias incidence has doubled. Chemical toxicants in the environment as well as poverty, racism, and inequitable access to medical care are factors known and suspected to contribute to causation of these pediatric diseases. Children are at risk of exposure to over 15,000 high-production-volume synthetic chemicals, nearly all of them developed in the past 50 years. These chemicals are used widely in consumer products and are dispersed in the environment. More than half are untested for toxicity. Children appear uniquely vulnerable to chemical toxicants because of their disproportionately heavy exposures and their inherent biological susceptibility. To prevent disease of environmental origin in America's children, the Children's Environmental Health Network (CEHN) calls for a comprehensive, national, child-centered agenda. This agenda must recognize children's vulnerabilities to environmental toxicants. It must encompass a) a new prevention-oriented research focus; b) a new child-centered paradigm for health risk assessment and policy formulation; and c) a campaign to educate the public, health professionals, and policy makers that environmental disease is caused by preventable exposures and is therefore avoidable. To anchor the agenda, CEHN calls for long-term, stable investment and for creation of a national network of pediatric environmental health research and prevention centers.

Child↗
PubMed1997

Prenatal care and infant lead exposure.

OBJECTIVE: The objective of the study was to determine the relation between prenatal care of mothers and blood lead concentrations in their offspring in the first year of life. METHODS: A retrospective survey was conducted of 200 predominantly black infants between the ages of 6 and 22 months (mean age, 13.4 months). The infants had been screened for the first time since birth at the Charleston County (South Carolina) Health Department. They resided in a neighborhood with the highest prevalence of lead poisoning in Charleston. Prenatal care use data were obtained after matching birth records with lead-screening records. RESULTS: Seventy-three infants (37%) had blood lead levels 0.48 micromol/L (> or = 10 microg/dl) or higher. Adequacy of prenatal care, defined by the Modified Kessner Index, showed 11% with intensive care (26% of these with high lead levels), 39% with adequate care (35% high blood lead levels), 35% with intermediate care (40% with high blood lead levels), 13% with inadequate care (42% with high blood lead levels), and 2% with no prenatal care (25% with high blood lead levels). With the exception of the small group with no prenatal care (n = 4), the proportion of infants with a high blood lead level was inversely proportional to the level of care. The logistic regression model that best fit the data included age at screen for lead and birth weight. Low birth weight babies (<2500 gm) were more likely to have a high blood lead level at primary screen than babies who were heavier at birth (odds ratio, 2.60; p = 0.04), and the older the baby at screening, the greater the likelihood of a high blood lead level (odds ratio, 1.23; p = 0.01). There was a trend for black infants to have a high blood lead level more often than white infants (odds ratio, 3.05; p = 0.06). CONCLUSIONS: Less than adequate use of prenatal care may reflect an increase in risk factors contributing to lead exposure in infancy. Low birth weight also was related to high blood lead levels. Further studies are required to differentiate among several hypotheses for this effect. Intrauterine lead exposure, which is known to reduce birth weight, may contribute to measured blood lead levels at first screen. Alternatively, low birth weight may increase lead absorption and retention in infancy or may increase risk of lead exposure.

Analysis of Variance↗
PubMed1995

How should federal policy reflect recent research in the area of intrauterine exposure to environmental hazards?

Present policy neither evaluates nor adequately protects the fetus from the effects of intrauterine exposure to environmental hazards. Some examples are intrauterine lead and methylmercury exposure and intrauterine PCB exposures. A sound policy based on a few basic principles can be developed to protect the fetus from harm from intrauterine exposures.

Environmental Pollutants↗
PubMed1991

Association between third-year medical students' abilities to organize hypotheses about patients' problems and to order appropriate diagnostic tests.

The authors studied the abilities of three groups of third-year medical students (a total of 310) at two schools to order appropriate diagnostic tests and procedures for four cases studies. Each student was classified as "organized," "mixed," or "non-organized" based on the degree of organization of the approach the student used to list hypotheses for the two cases he or she was assigned. Analysis of variance revealed that the students in the organized and mixed groups spent significantly fewer dollars for inappropriate diagnostic evaluations than did the students in the non-organized group for three of the four cases (p less than .05). Analyses of the mean expenditures for all cases revealed that the students in the organized and mixed groups spent significantly fewer dollars for inappropriate evaluations than did the students in the non-organized group (p less than .05). The medical school that was teaching its students to organize hypotheses had more students in the organized group than expected for every case. The authors conclude that the ability of students to organize hypotheses is directly related to their ability to avoid increased expenditures for inappropriate diagnostic tests and procedures, and that organized thinking about patients' problems is a skill that can be taught.

Clinical Competence↗
PubMed1989

Pharmacokinetics of ranitidine in critically ill infants.

The pharmacokinetic parameters of ranitidine were studied following administration of a single intravenous dose in 9 critically ill infants. Ranitidine disposition was best described by a biphasic elimination curve. For 8 patients, the mean values for T1/2, apparent volume of distribution, and total body clearance were 2.09 h, 1.61 l/kg, and 13.93 ml/min/kg, respectively. Based on simulated steady-state concentration profiles, a dose of 0.7 mg/kg administered intravenously every 6 h should maintain serum levels above 40 ng/ml for 4.7 h of the dosing interval with a wide degree of variability.

Child, Preschool↗
PubMed1986

Association of amino levulinate dehydratase levels and ferrochelatase inhibition in childhood lead exposure.

The basis for the clinical variation in response to lead exposure in children is not well understood. We studied selected children from a large lead screening program in whom elevation of red cell protoporphyrin concentration (a measure of inhibition of the enzyme ferrochelatase) was markedly above or below average for a given blood lead level. We then measured the activity of the enzyme amino levulinate dehydratase in 306 of these children, and found that ALA-d activity was lower in children with higher protoporphyrin elevation, independent of the effects of lead. This observation, coupled with reports in the literature of families with ALA-d deficiencies and elevated red cell protoporphyrin values, makes likely a genetic basis for some of the variation in susceptibility to lead. The mechanism by which the two effects are associated remains unknown.

Adolescent↗
PubMed1983

Evaluation of regional and nonregional poison centers.

The purpose of this study was to determine whether regional poison centers handle a particular poisoning situation better than nonregional centers do. Informed consent was obtained from 15 regional and 15 nonregional poison centers. A case involving salicylate ingestion by a three-year-old child was presented twice (one day call and one night call) to each center. Those answering the phone at the regional centers asked more information-gathering questions than did those at the nonregional centers (P less than 0.01) and were more proficient in their history taking (P less than 0.01). Nonregional centers did not consider the potentially toxic ingestion (220 mg per kilogram of body weight) important enough to treat or were not willing to handle the poisoning in one third of the calls. The nonregional centers recommended manual stimulation to induce emesis in 30 per cent of the calls, whereas none of the regional centers recommended this treatment. Four calls to the nonregional centers resulted in recommendations of inappropriate emetics--e.g., saltwater, raw eggs, or mustard water. The chance of obtaining incorrect recommendations for poisoning treatment from the nonregional centers was determined to be nine times greater than that from the regional centers. Indications of intention to follow up were twice as frequent among regional as among nonregional centers. These data strongly suggest that regional poison centers provide better and more consistent poison information than do nonregional centers.

Child↗
PubMed1983

Acute chlordane intoxication.

This report describes a patient who accidentally ingested 215 g of chlordane in a liquid pesticide formulation. The patient experienced multiple acute clinical sequellae attributable to his acute intoxication, including vomiting, diarrhea, seizures, coma and respiratory failure. Upon initial presentation and during the recovery phase, blood and urine specimens were collected to measure the disposition and elimination of chlordane and its metabolites. Whole blood chlordane concentrations measured over the subsequent 49 days suggested a multicompartmental kinetic profile of chlordane distribution, with an approximate terminal elimination half-life of 34 days. Tissue samples obtained from this patient, during elective surgery 58 days post chlordane ingestion, revealed persistent high levels of chlordane related metabolites. This case illustrates the physiological distribution and elimination of chlordane and its related metabolite residues after acute intoxication in an adult patient. Such information is important to improve the clinical management of patients acutely exposed to potentially lethal levels of pesticides.

Chlordan↗
PubMed1982

Repetitive doses of activated charcoal in Dapsone poisoning in a child.

A case of Dapsone poisoning, treated by repetitive dosing with activated charcoal, is reported. This 18-month-old child showed remarkably rapid resolution of his symptoms with this mode of therapy, becoming symptom free in 64 h. This rapid improvement is attributed to interruption by activated charcoal of the enterohepatic circulation of Dapsone. This mode of therapy may be indicated for other compounds having an enterohepatic circulation.

Charcoal↗