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Biomedical subjects

R A Etzel

Publications and source records attributed to R A Etzel.

At least 19 recordsLinked to original sources
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↗
PubMed1995

Indoor air pollution.

Explore the source record for details and available documents.

Air Pollutants, Radioactive↗
PubMed1995

Unintentional deaths from carbon monoxide poisoning in New Mexico, 1980 to 1988. A comparison of medical examiner and national mortality data.

Carbon monoxide was the number 1 cause of poisoning deaths in the United States from 1980 through 1988, with the highest rates reported in the western states. We studied unintentional deaths from carbon monoxide poisoning in New Mexico during this period using the multiple-cause mortality files from the National Center for Health Statistics (NCHS) and data from the New Mexico Office of the Medical Investigator (OMI). We compared the nationally available NCHS data with the more detailed OMI data to determine the sensitivity of NCHS data for the surveillance of this preventable cause of death. The NCHS data were 88% sensitive in identifying deaths from unintentional carbon monoxide poisoning and had a positive predictive value of 81% when compared with OMI data. Half of the unintentional carbon monoxide-related deaths were attributable to a home heating mechanism of some sort, 46% involved motor vehicle exhaust, and at least 42% were associated with alcohol use. We conclude that available NCHS data are a sensitive source of surveillance information about unintentional deaths from carbon monoxide poisoning. Additional details about specific deaths can be obtained from medical examiner files when needed.

Accidents↗
PubMed1994

Exacerbations of childhood asthma and ozone pollution in Atlanta.

Asthma prevalence and mortality due to asthma have been increasing during the last decade, and both the rates and the increases in rates have been higher for blacks than whites and higher for children than adults. Whether environmental factors such as air pollution contribute to these increases is unknown. The purpose of this study was to examine the relationship between emergency visits to a hospital for childhood asthma and exposure to ozone in an indigent, predominantly black population. Data were collected by abstracting clinical records for all children with asthma or reactive airway disease in one public hospital during the summer of 1990. From June 1, 1990, to August 31, 1990, 609 visits were made by children aged 1 to 16 years to an emergency clinic for treatment of asthma or reactive airway disease. Monitoring data indicated that maximum ozone levels equalled or exceeded 0.11 ppm on 6 days during the study period. The average number of visits for asthma or reactive airway disease was 37% higher on the days after those 6 days (from 6:00 PM to 6:00 PM the next day) than on other days (95% CI, RR = 1.02-1.73). The results of the study suggest that among black children from low-income families, asthma may be exacerbated following periods of high ozone pollution.

Adolescent↗
PubMed1994

An evaluation of the relationship between self-report and biochemical measures of environmental tobacco smoke exposure.

To evaluate the relationship between self-reported exposure to environmental tobacco smoke and saliva cotinine concentrations, we studied 186 nonsmokers. Each participant completed an exposure questionnaire, kept a daily exposure diary for 7 days, and provided a saliva sample for cotinine analysis. Salivary cotinine concentrations were measured using gas chromatography/mass spectrometry. Of the volunteers, 30% lived with one or more smokers, and 84% were regularly exposed to smokers at work. Eighty-three percent of the volunteers had detectable saliva cotinine concentrations (> or = 0.5 ng/ml) (median = 1.1; range = 0.5-7.4 ng/ml). Cotinine concentrations were related to exposure in the household and at the workplace. Volunteers who lived with smokers had significantly higher cotinine levels (median = 1.0; range = < 0.5-7.4 ng/ml) than those who did not (median = < 0.5; range = < 0.5-4.7 ng/ml). Volunteers who reported regular exposure at work had higher cotinine levels (median = 0.8; range = < 0.5-7.4 ng/ml) than those who did not (median = < 0.5; range = < 0.5-3.0 ng/ml). Cotinine concentrations were predicted by a regression equation that included the number of smokers at home and work and the number of minutes of exposure recorded in the daily diary (r2 = 0.29).

Adolescent↗
PubMed1994

Volatile organic compounds in the blood of persons in Kuwait during the oil fires.

Between March and November of 1991, approximately 9000 workers from 43 different countries battled the burning oil wells in Kuwait. To document the exposure of persons in Kuwait during the oil well fires to volatile organic compounds (VOCs), we obtained samples of blood from 14 U.S. personnel in Kuwait City in May of 1991 (group I) and 40 American firefighters working in the oil fields in October of 1991 (group II). Concentrations of VOCs in group I and group II were compared with those of a random sample of 114 persons in the United States (reference group). The median concentrations of VOCs in group I were equal to or lower than those in the reference group. We found significant differences between the median concentrations of several VOCs in group II and the reference group. Median levels of ethylbenzene were about 10 times higher among group II than among the reference group (0.53 microgram/l vs 0.052 microgram/l). Median levels of benzene, m-/p-xylene, o-xylene, styrene, and toluene among group II were more than double those of the reference group. Although firefighters had higher median concentrations of VOCs than the reference group, those American personnel in Kuwait not involved in fighting the oil fires had concentrations of VOCs comparable to those in the reference group. Blood VOC measurements indicate a significant increase in exposure to VOCs in firefighters, but do not demonstrate this in personnel in Kuwait City.

Adult↗