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R A Etzel

Publications and source records attributed to R A Etzel.

At least 19 recordsLinked to original sources
PubMed1999

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.

Adult↗
PubMed1998

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.

Adolescent↗
PubMed1998

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.

Acute Disease↗
PubMed1998

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.

Animals↗
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

Reexamination of epidemic asthma in New Orleans, Louisiana, in relation to the presence of soy at the harbor.

Epidemic asthma occurred in New Orleans, Louisiana, in the 1950s and 1960s, but its causes were never fully understood. Subsequently, similar outbreaks of epidemic asthma in Barcelona, Spain, were shown to be caused by the release of soy dust at the harbor. To investigate whether airborne soy dust may have contributed to epidemic asthma in New Orleans, the authors examined historical data on vessel cargo from the New Orleans harbor together with data on emergency department visits for asthma, for the period from 1957 through 1968. Days on which there were 64 or more visits for asthma were twice as likely to have occurred on days when a vessel carrying soy was at the harbor (odds ratio (OR) = 2.3, 95% confidence interval (CI) 1.5-3.3). The association was stronger when the maximum wind speed was less than 12 miles/hour (19.3 km/hour) (OR = 4.0, 95% CI 2.1-7.7) and strongest when wind speeds were low and the prevailing winds were from the south or southwest, the direction of two grain elevators from the hospital (OR = 6.7, 95% CI 1.5-46.7). Various temporal and climatic factors that had been associated with the occurrence of asthma outbreaks did not appear to be important confounding factors. The association was specific to soy cargo; no association was observed between asthma-epidemic days and the presence of either wheat or corn in vessels at the harbor. The results of this analysis provide further evidence that ambient soy dust is very asthmogenic and that asthma morbidity in a community can be influenced by exposures in the ambient atmosphere.

Adult↗
PubMed1997

Blood benzene concentrations in workers exposed to oxygenated fuel in Fairbanks, Alaska.

OBJECTIVE: In November 1992 residents of Fairbanks, Alaska became concerned about the potential health effects of an oxygenated fuel program during which 15% (by volume) methyl tertiary butyl ether (MTBE) was added to gasoline. To address those concerns, we earlier completed a survey of occupational exposure to MTBE. We conducted a follow-up survey of workers' exposure to benzene from gasoline in Fairbanks. DESIGN: Cross-sectional exposure survey. METHODS: We examined blood concentrations of benzene from a convenience sample of workers taken in December 1992 during the oxygenated fuel program and from another convenience sample of workers taken in February 1993 after the program was suspended. RESULTS: In December, the median blood benzene concentration of samples taken from four mechanics after their workshift (postshift) was 1.32 micrograms/l (range, 0.84-2.61 micrograms/l), and seven nonmechanics (drivers and other garage workers) had a median postshift blood benzene concentration of 0.27 microgram/l (range, 0.09-0.45 microgram/l). In February, nine mechanics had a median postshift blood benzene concentration of 1.99 micrograms/l (range, 0.92-3.23 micrograms/l), and nine nonmechanics had a median postshift blood benzene concentration of 0.26 microgram/l (range, 0.2-0.46 microgram/l). CONCLUSION: Mechanics had higher blood benzene concentrations than did nonmechanics, but further study is needed to determine the impact of the oxygenated fuel program on exposure to benzene.

Benzene↗
PubMed1997

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.

Adrenergic beta-Agonists↗
PubMed1997

Environmental risk factors associated with pediatric idiopathic pulmonary hemorrhage and hemosiderosis in a Cleveland community.

BACKGROUND: Unexplained pulmonary hemorrhage and hemosiderosis are rarely seen in infancy. A geographic cluster of 10 infants with this illness was identified in a large pediatric referral hospital in Cleveland, Ohio, during the period of January 1993 through December 1994. One infant died of severe respiratory failure. METHODS: A case-control study was conducted. Three control infants were matched by age with each case infant. All study infants' guardians were interviewed. Questions were asked about child care practices and home conditions for the period before case infants' illnesses. All infants' records were reviewed, their homes were visited, and a structural and environmental survey was conducted. RESULTS: All 10 case infants were black, and 9 were male, whereas 50.0% of control infants were male, and 83.3% were black. The case infants' mean age was 10.2 weeks (range, 6 weeks to 6 months). Matched analysis demonstrated that case infants' homes were more likely to have had water damage preceding the pulmonary hemorrhage event (odds ratio, 16.25; 95% confidence interval, 2.55 to infinity). Case infants were also more likely to have had close relatives with pulmonary hemorrhage (odds ratio, 33.14; 95% confidence interval, 5.10 to infinity). In addition, 50.0% of case infants experienced recurrent pulmonary hemorrhaging after returning to their homes. CONCLUSION: The results of this investigation of a cluster of infants with massive, acute pulmonary hemorrhage and hemosiderosis suggest that the affected infants may have been exposed to contaminants in their homes. Epidemiologic clues, such as water damage in the case infants' homes, suggest that environmental risk factors may contribute to pulmonary hemorrhage.

Acute Disease↗
PubMed1997

Active and passive smoking: hazards for children.

This manuscript describes the tobacco industry's efforts to recruit active smokers among the adolescent population, the effects of environmental tobacco smoke on nonsmokers, and lists some steps pediatricians can take to influence smoking behavior. Six health effects result from passive smoking. Children exposed to environmental tobacco smoke have increased lower respiratory illness rates, especially in the first year of life, passive smoking is associated with increased rates of chronic middle ear effusion in children. Exposure to cigarette smoke is associated with small changes in pulmonary function. Exposure to environmental tobacco smoke increases an asthmatic child's exacerbations. Exposure to environmental tobacco smoke is a risk factor for sudden infant death syndrome. Passive exposure during childhood to a parents smoking increases a child's risk of leukemia and lymphoma during adulthood. Pediatricians and others who care for children must try to limit as much as possible, the exposure of children to the cigarette smoke produced by others.

Adolescent↗
PubMed1996

Exposure of the US population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey, 1988 to 1991.

OBJECTIVE: To estimate the extent of exposure of the US population to environmental tobacco smoke and the contribution of the home and workplace environment to environmental tobacco smoke exposure. DESIGN: Nationally representative cross-sectional survey including questionnaire information from persons aged 2 months and older (n=16818) and measurements of serum cotinine (a metabolite of nicotine) from persons aged 4 years and older (n=10642). SETTING/PARTICIPANTS: Participants in the Third National Health and Nutrition Examination Survey, October 25, 1988, to October 21, 1991. RESULTS: Of US children aged 2 months to 11 years, 43% lived in a home with at least 1 smoker, and 37% of adult non-tobacco users lived in a home with at least 1 smoker or reported environmental tobacco smoke exposure at work. Serum cotinine levels indicated more widespread exposure to nictoine. Of non-tobacco users, 87.9% had detectable levels of serum cotinine. Both the number of smokers in the household and the hours exposed at work were significantly and independently associated (P<.001, multiple regression t test) with increased serum cotinine levels. Serum cotinine levels of children, non-Hispanic blacks, and males indicated that these groups had higher exposure to environmental tobacco smoke. Dietary variables showed no consistent association with serum cotinine levels, and dietary contribution to serum cotinine level, if any, appeared to be extremely small. CONCLUSIONS: The high proportion of the population with detectable serum cotinine levels indicates widespread exposure to environmental tobacco smoke in the US population. Both the home and workplace environments significantly contribute to environmental tobacco smoke exposure in the United States.

Adolescent↗
PubMed1996

Mercury exposure in high school chemistry teachers.

To assess whether high school chemistry teachers had higher urinary mercury concentrations than other high school teachers, 24 high school teachers from nine schools in northeastern Ohio were studied. First morning voided urine samples and air samples from the teachers' classrooms were analyzed for total mercury content by cold vapor atomic absorption. The median adjusted urinary mercury concentration in the 12 chemistry teachers was 4.6 microg/g creatinine (range 2.2-8.2 microg/g creatinine) and it was 6.3 microg/g creatinine in the 12 non-chemistry teachers. All classroom air samples contained mercury levels below detection limits. No evidence was provided that high school chemistry teachers are at increased risk of chronic mercury exposure from their teaching activities compared to other high school teachers.

Adult↗
PubMed1996

Toxigenic molds in water-damaged buildings: dechlorogriseofulvins from Memnoniella echinata.

An investigation of a cluster of cases of pulmonary hemosiderosis in infants in Cleveland, OH, led to the isolation of many isolates of Stachybotrys atra and two isolates of a related toxigenic fungus, Memnoniella echinata. M. echinata produces two cytotoxic trichothecene mycotoxins, trichodermol (1a) and trichodermin (1b), as well as several griseofulvins. Dechlorogriseofulvin (2a) and epidechlorogriseofulvin (2b) were the major compounds isolated. This is the first report of a fungus outside the Penicillium genus producing griseofulvins.

Griseofulvin↗
PubMed1996

Pulmonary fibrosis deaths in the United States, 1979-1991. An analysis of multiple-cause mortality data.

We sought to describe pulmonary fibrosis mortality in the United States from 1979 through 1991 by analyzing death certificate reports compiled by the National Center for Health Statistics. Of the 26,866,600 people who died during the study period, 107,292 had a diagnosis of pulmonary fibrosis listed on their death certificates. Among men, age-adjusted mortality rates increased from 48.6 per 1,000,000 in 1979 to 50.9 per 1,000,000 in 1991 and, among women, these rates increased from 21.4 per 1,000,000 in 1979 to 27.2 per 1,000,000 in 1991. Among both men and women rates were higher in older age strata than in younger age strata. Age-adjusted mortality rates were consistently higher among whites and people of races than blacks. The frequency with which pulmonary fibrosis was listed as the underlying cause of death increased from 40% in 1979 to 56% in 1991. Age-adjusted mortality rates varied by state, with lowest rates in the Midwest and Northeast, and the highest rates in the West and Southeast. We conclude that the age-adjusted rate of pulmonary fibrosis among decedents in the United States increased, and pulmonary fibrosis was listed as the underlying cause of death with increasing frequency, over the study period. We cannot determine whether the differences we detected between regions, sexes, and races are related to characteristics of the disease or problems in death certification and coding.

Adolescent↗
PubMed1996

Effects of air pollution on the respiratory health of asthmatic children living in Mexico City.

The relation between air pollution and the exacerbation of childhood asthma was studied in a panel of 71 children (aged 5 to 7 yr) with mild asthma who resided in the northern part of mexico City. During the follow-up, ambient measures of particulate matter less than 10 microns (PM10, 24-h average) and ozone (1-h maximum) frequently exceeded the Mexican standards for these contaminants. The peak expiratory flow rate (PEFR) was strongly associated with PM10 levels and marginally with ozone levels. Respiratory symptoms (coughing, phlegm production, wheezing, and difficulty breathing) were associated with both PM10 and ozone levels. An increase of 20 micrograms/m3 of PM10 was related to an 8% increase in lower respiratory illness (LRI) among children on the same day (95% confidence interval [CI] = 1.04-1.15), and an increase of 10 micrograms/m3 in the weekly mean of particulate matter less than 2.5 microns (PM2.5) was related to a 21% increase in LRI (95% CI = 1.08-1.35). A 50 parts per billion (ppb) increase in ozone was associated with a 9% increase in LRI (95% CI = 1.03-1.15) on the same day. We concluded that children with mild asthma are affected by the high ambient levels of particulate matter and ozone observed in the northern part of Mexico City.

Air Pollutants↗
PubMed1995

Effects of urban air pollutants on emergency visits for childhood asthma in Mexico City.

The metropolitan area of Mexico City, Mexico, has serious air pollution problems. Although air contaminants may contribute to clinical asthma, there are at present no data on the relation between air pollution exposure and childhood asthma in Mexico City. The authors reviewed data on emergency visits from January to June 1990 at one major pediatric hospital in Mexico City. They used a Poisson regression model to study the relation between the number of daily emergency visits for asthma and air pollutant levels. The levels of ozone and sulfur dioxide-exposure were significantly associated with the number of emergency visits for asthma. After adjustment for potential confounding factors, the multivariate regression model predicted that an increase of 50 ppb in the 1-hour maximum ozone level would lead to a 43% increase in the number of emergency visits for asthma on the following day. Exposure to high ozone levels (> 110 ppb) for 2 consecutive days increased the number of asthma-related emergency visits by 68 percent. The results of this study suggest that ozone exposure is positively associated with the number of children's emergency visits for asthma in Mexico City.

Adolescent↗
PubMed1995

Indoor air pollution and childhood asthma: effective environmental interventions.

Exposure to indoor air pollutants such as tobacco smoke and dust mites may exacerbate childhood asthma. Environmental interventions to reduce exposures to these pollutants can help prevent exacerbations of the disease. Among the most important interventions is the elimination of environmental tobacco smoke from the environments of children with asthma. However, the effectiveness of reducing asthmatic children's exposure to environmental tobacco smoke on the severity of their symptoms has not yet been systematically evaluated. Dust mite reduction is another helpful environmental intervention. This can be achieved by enclosing the child's mattresses, blankets, and pillows in zippered polyurethane-coated casings. Primary prevention of asthma is not as well understood. It is anticipated that efforts to reduce smoking during pregnancy could reduce the incidence of asthma in children. European studies have suggested that reducing exposure to food and house dust mite antigens during lactation and for the first 12 months of life diminishes the development of allergic disorders in infants with high total IgE in the cord blood and a family history of atopy. Many children with asthma and their families are not receiving adequate counseling about environmental interventions from health care providers or other sources.

Air Pollution, Indoor↗