Scatter radiation reduction with a radiation-absorbing pad in interventional radiology examinations.

PURPOSE: Radiation-absorbing pads are an additional possibility to reduce scattered radiation at its source. The goal of this study is to investigate the efficacy of a new reusable radiation-absorbing pad at its origin in an experimental setup. MATERIAL AND METHODS: All measurements were carried out using a clinical angiography system with a standardized fluoroscopy protocol, different C-arm angulations and an anthropomorphic torso phantom as a scattering body. An ionization chamber was used to measure the radiation exposure at five different heights of a simulated operator during a simulated transfemoral angiography intervention. Measurements were carried out with and without radiation-absorbing pads with lead equivalents of 0.25 and 0.5 mm placed onto the scattering body. For all measurements a mobile acrylic shield and an under-table lead curtain was used. RESULTS: At all operator heights from 100 to 165 cm a significant radiation dose reduction of up to 80.6 % (p < 0.01) using the radiation-absorbing pad was measured, when compared to no radiation-absorbing pad. At the height of 165 cm the radiation-absorbing pad with a lead equivalence of 0.5 mm showed a significant radiation dose reduction (51.4 %, p < 0.01) in comparison to a lead equivalence of 0.25 mm. CONCLUSION: The addition of a radiation-absorbing pad to the standard protection means results in a significant dose reduction for the operator, particularly for upper body parts.

Protective Efficacy of Different Ocular Radiation Protection Devices: A Phantom Study.

PURPOSE: The aim of this study was to investigate the efficacy of different designs and types of ocular radiation protection devices depending on simulated varied body heights in a phantom-simulated thoracic intervention. MATERIALS AND METHODS: A clinical angiography system with a standardized fluoroscopy protocol with an anthropomorphic chest phantom as a scattering object and optically stimulated luminescence dosimeters for measuring radiation dose were used. The dosimeters were placed at the position of eyes of an anthropomorphic head phantom simulating the examiner. The head phantom was placed on a height-adjustable stand simulating the height of the examiner from 160 to 200 cm with 10 cm increments. The dose values were then measured with no radiation protection, a weightless-like radiation protection garment, radiation protection glasses and visors. RESULTS: The average dose reduction using radiation protection devices varied between 57.7 and 83.4% (p < 0.05) in comparison with no radiation protection. Some radiation protection glasses and visors showed a significant dose reduction for the eye lenses when the height of the examiner increased. The right eye was partially less protected, especially if the distances between the simulated examiner's head and the scatter object were small. CONCLUSION: All the investigated protection devices showed a significant reduction in radiation exposure to the simulated examiner. For some devices, the radiation dose increased with decreasing distance to the scattering object, especially for the right eye lens.

Indoor air pollutants in homes and schools.

Exposure to the four indoor air pollutants mentioned in this article may cause illnesses and fatalities in children. It is important for pediatricians to be aware of each of them and to remove children from environments contaminated with these pollutants. Guidance about monitoring the indoor air and interpreting the results is difficult to find. A chart of proposed guidelines may help the pediatrician faced with an indoor air problem (Table 1).

Serotype distribution of Salmonella isolates from food animals after slaughter differs from that of isolates found in humans.

If raw meat and poultry are the primary point of entry for Salmonella species into human populations, a correlation might be expected between the serotype distribution of Salmonella species isolated from animals at the time of slaughter and that of isolates found in humans. For 1990-1996, sufficient national data were available to permit such a comparison. A mathematical model was developed to predict serotype distributions of Salmonella isolates among humans on the basis of animal data. There was a significant mismatch between the serotype distributions among humans predicted by the model and those actually observed. This mismatch raises questions about the validity of the "standard" assumptions about Salmonella transmission on which the model was based-namely, that raw animal products are the primary source for human salmonellosis, that the risk of transmission to humans is equal for all food product categories, and that all Salmonella serotypes have an equal ability to cause human illness.

Incidence of foodborne illnesses reported by the foodborne diseases active surveillance network (FoodNet)-1997. FoodNet Working Group.

In 1997, the Foodborne Diseases Active Surveillance Program (FoodNet) conducted active surveillance for culture-confirmed cases of Campylobacter, Escherichia coli O157, Listeria, Salmonella, Shigella, Vibrio, Yersinia, Cyclospora, and Cryptosporidium in five Emerging Infections Program sites. FoodNet is a collaborative effort of the Centers for Disease Control and Prevention's National Center for Infectious Diseases, the United States Department of Agriculture's Food Safety and Inspection Service, the Food and Drug Administration's Center for Food Safety and Applied Nutrition, and state health departments in California, Connecticut, Georgia, Minnesota, and Oregon. The population under active surveillance for foodborne infections was approximately 16.1 million persons or roughly 6% of the United States Population. Through weekly or monthly contact with all clinical laboratories in these sites, 8,576 total isolations were recorded: 2,205 cases of salmonellosis, 1,273 cases of shigellosis, 468 cases of cryptosporidiosis, 340 of E. coli O157:H7 infections, 139 of yersiniosis, 77 of listeriosis, 51 of Vibrio infections, and 49 of cyclosporiasis. Results from 1997 demonstrate that while there are regional and seasonal differences in reported incidence rates of certain bacterial and parasitic diseases, and that some pathogens showed a change in incidence from 1996, the overall incidence of illness caused by pathogens under surveillance was stable. More data over more years are needed to assess if observed variations in incidence reflect yearly fluctuations or true changes in the burden of foodborne illness.

Workshop to identify critical windows of exposure for children's health: immune and respiratory systems work group summary.

Fetuses, infants, and juveniles (preadults) should not be considered simply "small adults" when it comes to toxicological risk. We present specific examples of developmental toxicants that are more toxic to children than to adults, focusing on effects on the immune and respiratory systems. We describe differences in both the pharmacokinetics of the developing immune and respiratory systems as well as changes in target organ sensitivities to toxicants. Differential windows of vulnerability during development are identified in the context of available animal models. We provide specific approaches to directly investigate differential windows of vulnerability. These approaches are based on fundamental developmental biology and the existence of discrete developmental processes within the immune and respiratory systems. The processes are likely to influence differential developmental susceptibility to toxicants, resulting in lifelong toxicological changes. We also provide a template for comparative research. Finally, we discuss the application of these data to risk assessment.

Cardiopulmonary baroreceptor control of muscle sympathetic nerve activity in heat-stressed humans.

Whole body heating decreases central venous pressure (CVP) while increasing muscle sympathetic nerve activity (MSNA). In normothermia, similar decreases in CVP elevate MSNA, presumably via cardiopulmonary baroreceptor unloading. The purpose of this project was to identify whether increases in MSNA during whole body heating could be attributed to cardiopulmonary baroreceptor unloading coincident with the thermal challenge. Seven subjects were exposed to whole body heating while sublingual temperature, skin blood flow, heart rate, arterial blood pressure, and MSNA were monitored. During the heat stress, 15 ml/kg warmed saline was infused intravenously over 7-10 min to increase CVP and load the cardiopulmonary baroreceptors. We reported previously that this amount of saline was sufficient to return CVP to pre-heat stress levels. Whole body heating increased MSNA from 25 +/- 3 to 39 +/- 3 bursts/min (P < 0. 05). Central blood volume expansion via rapid saline infusion did not significantly decrease MSNA (44 +/- 4 bursts/min, P > 0.05 relative to heat stress period) and did not alter mean arterial blood pressure (MAP) or pulse pressure. To identify whether arterial baroreceptor loading decreases MSNA during heat stress, in a separate protocol MAP was elevated via steady-state infusion of phenylephrine during whole body heating. Increasing MAP from 82 +/- 3 to 93 +/- 4 mmHg (P < 0.05) caused MSNA to decrease from 36 +/- 3 to 15 +/- 4 bursts/min (P < 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating is not the primary mechanism resulting in elevations in MSNA. Moreover, arterial baroreceptors remain capable of modulating MSNA during heat stress.

Air pollution and bronchitic symptoms in Southern California children with asthma.

People who live in cities with dirty air have blacker lungs than people who live in rural areas with less air pollution. This is because, although particulates larger than 10 microm are filtered out when inhaled air passes through the nose, smaller particulates reach the lower airways. The particulates that reach the alveoli (the terminal air pockets of the lungs) stay there permanently. This accounts for the fact that a person who has lived in a polluted city for many years has blacker lungs than one who has lived in a polluted city for a shorter time.

Indoor mold and Children's health

Reactive airways disease in children is increasing in many countries around the world. The clinical diagnosis of asthma or reactive airways disease includes a variable airflow and an increased sensitivity in the airways. This condition can develop after an augmented reaction to a specific agent (allergen) and may cause a life-threatening situation within a very short period of exposure. It can also develop after a long-term exposure to irritating agents that cause an inflammation in the airways in the absence of an allergen. (paragraph) Several environmental agents have been shown to be associated with the increased incidence of childhood asthma. They include allergens, cat dander, outdoor as well as indoor air pollution, cooking fumes, and infections. There is, however, increasing evidence that mold growth indoors in damp buildings is an important risk factor. About 30 investigations from various countries around the world have demonstrated a close relationship between living in damp homes or homes with mold growth, and the extent of adverse respiratory symptoms in children. Some studies show a relation between dampness/mold and objective measures of lung function. Apart from airways symptoms, some studies demonstrate the presence of general symptoms that include fatigue and headache and symptoms from the central nervous system. At excessive exposures, an increased risk for hemorraghic pneumonia and death among infants has been reported. (paragraph) The described effects may have important consequences for children in the early years of life. A child's immune system is developing from birth to adolescence and requires a natural, physiologic stimulation with antigens as well as inflammatory agents. Any disturbances of this normal maturing process will increase the risk for abnormal reactions to inhaled antigens and inflammagenic agents in the environment. (paragraph) The knowledge about health risks due to mold exposure is not widespread and health authorities in some countries may not be aware of the serious reactions mold exposure can provoke in some children. Individual physicians may have difficulty handling the patients because of the lack of recognition of the relationship between the often complex symptoms and the indoor environment (paragraph) The workshop was organized to develop a basis for risk assessment and formulation of recommendations, particularly for diagnostic purposes and prevention, and to formulate priorities for future research. The participants were all active researchers with current experience in child health, molds, and respiratory disease. They were engaged in free and intensive discussions on a scientific basis throughout the duration of the 3-day workshop (paragraph) This monograph contains peer-reviewed papers based on individual presentations at the workshop as well as the workshop conclusions. They are offered to the public health community, administrators, research agencies, physicians, particularly pediatricians, nurses and health workers as information and encouragement to engage themselves in this health problem of importance for the next generation in our population. (paragraph) Acknowledgments: The workshop received financial support from the U.S. Environmental Protection Agency, the National Center for Environmental Assessment at the U.S. EPA, the Vardal Foundation (Sweden), Astra Corp (Sweden), the Committee on Organic Dusts, International Commission on Occupational Health. The printing of this document was made possible by a grant from the Center for Indoor Air Research (U.S.). Yvonne Peterson, research secretary, provided excellent and invaluable assistance in the organization and publication efforts.

Introduction and summary: workshop on children's health and indoor mold exposure.

To evaluate the health consequences for children of indoor exposure to molds, an international workshop was organized with 15 scientists from eight countries. The participants agreed that exposure to molds may constitute a health threat to children resulting in respiratory symptoms in both the upper and lower airways, an increased incidence of infections, and skin symptoms. Allergy, either to molds or to other indoor agents, also presents a health risk. At very high exposure levels to specific molds, nose bleeding, hemoptysis, and pulmonary hemorrhage have been documented. Pediatricians and allergists need to obtain information about mold and dampness in the home environment when examining children with chronic respiratory symptoms, recurrent infections, or persistent fatigue and headache. Measurement techniques are available to determine exposure. Most important, the source of dampness must be eliminated and the indoor environment must be thoroughly cleaned of molds.

Overview of investigations into pulmonary hemorrhage among infants in Cleveland, Ohio.

Idiopathic pulmonary hemorrhage was diagnosed in 37 infants in the Cleveland, Ohio, area between 1993 and 1998. This rare disorder has been related to 12 deaths, including 7 originally thought to be sudden infant death syndrome. Thirty of the infants were African American, all of whom lived in a limited geographic area of eastern metropolitan Cleveland, an area of older housing stock. An investigation led by the Centers for Disease Control and Prevention has found an association with household exposure to a toxigenic mold, Stachybotrys chartarum, and other fungi. The rapidly growing lungs of young infants appear to be especially vulnerable to the toxins made by toxigenic molds. Environmental tobacco smoke was frequently present in the infants' homes and may be a trigger precipitating the acute bleeding. Stachybotrys, although not thought to be a common mold, is known to have a wide geographic distribution. An additional 101 cases of acute, idiopathic pulmonary hemorrhage have been reported in infants in the United States over the past 5 years. In this overview, the investigations are summarized, the clinical profile is described, the toxicity of S. chartarum is discussed, and pathophysiologic concepts are presented.

Effect of increasing central venous pressure during passive heating on skin blood flow.

Whole body heating in humans increases skin blood flow (SkBF) and decreases central venous pressure (CVP). This study sought to identify whether elevations in SkBF are augmented during passive heating if CVP is increased during the heat stress. Seven subjects were exposed to passive heating. Once SkBF was substantially elevated, 15 ml/kg warm saline were rapidly infused intravenously. Whole body heating significantly increased cutaneous vascular conductance and decreased CVP from 7.7 +/- 0.6 to 4.9 +/- 0.5 mmHg (P < 0.05). Saline infusion returned CVP to pre-heat-stress pressures (7.9 +/- 0.6 mmHg; P > 0.05) and significantly increased cutaneous vascular conductance relative to the period before saline administration. Moreover, saline infusion did not alter mean arterial pressure, pulse pressure, or esophageal temperature (all P > 0.05). To serve as a volume control, 15 ml/kg saline were rapidly infused intravenously in normothermic subjects. Saline infusion increased CVP (P < 0.05) without affecting mean arterial pressure, pulse pressure, or cutaneous vascular conductance (all P > 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating may attenuate the elevation in SkBF in humans, whereas loading cardiopulmonary baroreceptors in normothermia has no effect on SkBF.

Study of toxin production by isolates of Stachybotrys chartarum and Memnoniella echinata isolated during a study of pulmonary hemosiderosis in infants.

A cluster of cases of pulmonary hemosiderosis among infants was reported in Cleveland, Ohio, during 1993 and 1994. These unusual cases appeared only in infants ranging in age from 1 to 8 months and were characterized by pulmonary hemorrhage, which caused the babies to cough up blood. A case-control study identified major home water damage (from plumbing leaks, roof leaks, or flooding) as a risk factor for development of pulmonary hemorrhage in these infants. Because of an interest in the possibility that trichothecene mycotoxins might be involved in this illness, a number of isolates of Stachybotrys chartarum were grown in the laboratory on rice, and extracts were prepared and analyzed both for cytotoxicity and for specific toxins. Two isolates of Memnoniella echinata, a fungus closely related to S. chartarum, were also included in these studies. S. chartarum isolates collected from the homes were shown to produce a number of highly toxic compounds, and the profiles of toxic compounds from M. echinata were similar; the most notable difference was the fact that the principal metabolites produced by M. echinata were griseofulvins.

Acute pulmonary hemorrhage in infants associated with exposure to Stachybotrys atra and other fungi.

BACKGROUND: A geographic cluster of 10 cases of pulmonary hemorrhage and hemosiderosis in infants occurred in Cleveland, Ohio, between January 1993 and December 1994. STUDY DESIGN: This community-based case-control study tested the hypothesis that the 10 infants with pulmonary hemorrhage and hemosiderosis were more likely to live in homes where Stachybotrys atra was present than were 30 age- and ZIP code-matched control infants. We investigated the infants' home environments using bioaerosol sampling methods, with specific attention to S atra. Air and surface samples were collected from the room where the infant was reported to have spent the most time. RESULTS: Mean colony counts for all fungi averaged 29 227 colony-forming units (CFU)/m3 in homes of patients and 707 CFU/m3 in homes of controls. The mean concentration of S atra in the air was 43 CFU/m3 in homes of patients and 4 CFU/m3 in homes of controls. Viable S atra was detected in filter cassette samples of the air in the homes of 5 of 9 patients and 4 of 27 controls. The matched odds ratio for a change of 10 units in the mean concentration of S atra in the air was 9.83 (95% confidence interval, 1.08-3 X 10(6)). The mean concentration of S atra on surfaces was 20 X 10(6) CFU/g and 0.007 x 10(6) CFU/g in homes of patients and controls, respectively. CONCLUSION: Infants with pulmonary hemorrhage and hemosiderosis were more likely than controls to live in homes with toxigenic S atra and other fungi in the indoor air.

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.

Exposure to environmental tobacco smoke and risk factors for heart disease among never smokers in the Third National Health and Nutrition Examination Survey.

The relative risk of coronary artery disease among never smokers exposed to environmental tobacco smoke (ETS) versus never smokers not exposed to ETS is approximately 1.2 based on more than a dozen epidemiologic studies. Most of these studies have controlled for the major heart disease risk factors, but residual or uncontrolled confounding remains a possible explanation for the epidemiologic findings. The authors studied 3,338 never-smoking adults aged 17 years or older, who are representative of all US never smokers, in the 1988-1991 Third National Health and Nutrition Examination Survey (NHANES III) to determine whether selected risk factors for heart disease differ between ETS-exposed and -nonexposed persons. Both self-reported ETS exposure (at home and at work) and serum cotinine levels were available, the latter reflecting recent ETS exposure. After adjustments were made for age, sex, race, and education among adults aged 17 years or older, no significant differences were found between the ETS exposed and the nonexposed for any of 13 cardiovascular risk factors with the exception of dietary carotene, which was lower among the exposed. On the other hand, significant positive linear trends were found between serum cotinine and two risk factors (body mass index and alcohol consumption), and significant inverse trends were found with dietary carotene. There were also few differences between exposed and nonexposed never smokers among adults aged 40 years or older, who are most at risk of heart disease. In this group, however, there was an inverse linear trend between serum cotinine and high density lipoprotein cholesterol (p < 0.001). This finding could result from ETS exposure rather than be an indication of confounding; a similar inverse trend was found for children, confirming other results in the literature. Overall, these data suggest little potential for confounding by the heart disease risk factors studied here when ETS exposure is determined by self-report.

Evidence of functional beta-adrenoceptors in the cutaneous vasculature.

During a hyperthermic challenge, skin blood flow (SkBF) increases primarily through activation of the cutaneous active vasodilator system. However, mechanisms through which activation of this system elevates SkBF remain unknown. In this project, we sought to identify whether functional beta-adrenoceptors exist on cutaneous vessels and, if present, whether these receptors play an important role in elevating SkBF during a hyperthermic challenge. In protocol 1, SkBF was assessed over two intradermal microdialysis probes. Initially, both probes were perfused with lactated Ringer solution. Probe A was then perfused with a 200 microM solution of the beta-adrenoceptor agonist isoproterenol while probe B was perfused with a 1.7 mM solution of the beta-adrenoceptor antagonist propranolol. Isoproterenol perfusion significantly increased SkBF from 17.7 +/- 2.4 to 70.8 +/- 13.2 perfusion units (PU; P < 0.05), whereas propranolol perfusion did not significantly affect SkBF (23.4 +/- 6.5 to 27.0 +/- 6.8 PU; P > 0.05). After this period, the solutions perfusing the probes were switched. Isoproterenol did not significantly change SkBF at the propranolol-treated site (27.0 +/- 6.8 to 26.4 +/- 7.5 PU; P < 0.05). In protocol 2, SkBF was assessed over two microdialysis probes during indirect whole body heating. One probe was perfused with Ringer solution while the other probe was perfused with 1.7 mM propranolol. The degree of elevation in SkBF during heat stress at the propranolol-treated site (10.4 +/- 1.5 to 35.8 +/- 3.1 PU) was similar to the elevation in SkBF at the Ringer solution site (11.6 +/- 1.0 to 35.0 +/- 1.2 PU). These data demonstrate the presence of functional beta-adrenoceptors in the skin; however, these receptors play no significant role in mediating cutaneous vasodilation during indirect whole body heating.