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Biomedical subjects

F Holguin

Publications and source records attributed to F Holguin.

5 recordsLinked to original sources
PubMed2005

Risk factors for prevalence of and mortality related to restriction on spirometry: findings from the First National Health and Nutrition Examination Survey and follow-up.

OBJECTIVE: To define risk factors for both restriction on spirometry and subsequent mortality in a national cohort of US adults. METHODS: Participants in the First National Health and Nutrition Examination Survey (NHANES I) were followed for up to 22 years. Subjects were classified using the forced expiratory volume in one second (FEV1), the forced vital capacity (FVC), and the FEV1/FVC ratio into subgroups with and without restriction on spirometry. Regression models were developed to determine risk factors for restriction on spirometry and death. RESULTS: Our final cohort consisted of 4320 subjects, of whom 481 (10.3 weighted %) had restriction on spirometry. The largest risk factors for restriction on spirometry were a cardiothoracic ratio of >55% (OR 4.3, 95%CI 3.1-5.9), race other than black or white (OR 3.7, 95%CI 1.8-7.8), and a history of stroke or paralysis (OR 1.8, 95%CI 1.1-2.9). The overall mortality rate was increased in subjects with restriction on spirometry (25.7 vs. 10.3 deaths per 1000 person-years). CONCLUSIONS: Restriction on spirometry is associated with comorbid disease and increased mortality, and is present in a significant proportion of the population.

Adult↗
PubMed2004

Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey.

BACKGROUND: A study was undertaken to determine the relation between urinary cadmium levels and lung function in a nationally representative cohort of current, former, and never smokers in the US. Urinary cadmium levels reflect the total body burden of cadmium. METHODS: The following data from the Third National Health and Nutrition Examination Survey were analysed: urinary cadmium (adjusted for urinary creatinine), lung function, sex, race/ethnicity, age, education level, job category, body mass index, serum cotinine level, and smoking history. Linear regression models were developed to predict lung function using urinary cadmium as the main predictor, adjusting for other covariates and stratified by smoking status. RESULTS: Data were available on 16 024 adults. Current smokers had higher mean (SE) urinary cadmium/creatinine levels (0.46 (0.01) micro g/g) than former (0.32 (0.01) micro g/g) or never smokers (0.23 (0.01) micro g/g). Higher levels of urinary cadmium were associated with significantly lower forced expiratory volumes in 1 second (FEV(1)) in current (-2.06%, 95% confidence interval (CI) -2.86 to -1.26 per 1 log increase in urinary cadmium) and former smokers (-1.95%, 95% CI -2.87 to -1.03) but not in never smokers (-0.18%, 95% CI -0.60 to 0.24). Similar results were obtained for forced vital capacity (FVC) and FEV(1)/FVC. CONCLUSIONS: Cadmium, which is known to cause emphysema in occupational settings, may also be important in the development of tobacco related lung disease.

Adolescent↗
PubMed2004

Risk factors for asthma incidence. A review of recent prospective evidence.

AIM: The aim of this study is to determine what factors have been shown, in prospective studies, to predict the incidence of asthma. METHODS: We performed a systematic review of peer-reviewed literature from 1994 to 2004 to determine what factors predict the development of asthma in both children and adults. This search strategy yielded 40 studies, with 36 providing some estimate of asthma incidence for the total sample and or a specific subgroup. RESULTS: Annual estimated incidence of physician-diagnosed asthma ranged from 0.6 to 29.5 per 1000 persons. Risk factors for incident asthma among children included: male sex, atopic sensitization, parental history of asthma, early-life stressors and infections, obesity, and exposure to indoor allergens, tobacco smoke and outdoor pollutants. Risk factors for adult-onset asthma included female sex, airway hyperresponsiveness, lifestyle factors, and work-related exposures. CONCLUSION: Risk factors for asthma include both modifiable and nonmodifiable ones, and they vary between children and adults. This review of prospective evidence supports tobacco and smoke avoidance as an intervention for the primary prevention of childhood asthma. During adolescence and adulthood, targeting lifestyle factors like obesity and smoking or reducing occupational exposures are the best opportunities for asthma prevention. Before specific public health recommendations can be made, however, additional longitudinal research is needed to better characterize target populations and identify appropriate settings for multifaceted asthma interventions.

Asthma↗
PubMed1998

Chronic ethanol ingestion impairs alveolar type II cell glutathione homeostasis and function and predisposes to endotoxin-mediated acute edematous lung injury in rats.

Chronic alcohol abuse increases the incidence and mortality of the acute respiratory distress syndrome (ARDS) in septic patients. To examine a potential mechanism, we hypothesized that ethanol ingestion predisposes to sepsis-mediated acute lung injury by decreasing alveolar type II cell glutathione homeostasis and function. Lungs isolated from rats fed ethanol (20% in water for >/= 3 wk), compared with lungs from control-fed rats, had greater (P < 0. 05) edematous injury (reflected by nonhydrostatic weight gain) after endotoxin (2 mg/kg intraperitoneally) and subsequent perfusion ex vivo with n-formylmethionylleucylphenylalanine (fMLP, 10(-7) M). Ethanol ingestion decreased (P < 0.05) glutathione levels in the plasma, lung tissue, and lung lavage fluid, and increased (P < 0.05) oxidized glutathione levels in the lung lavage fluid. Furthermore, ethanol ingestion decreased type II cell glutathione content by 95% (P < 0.05), decreased (P < 0.05) type II cell surfactant synthesis and secretion, and decreased (P < 0.05) type II cell viability, in vitro. Finally, treatment with the glutathione precursors S-adenosyl-L-methionine and N-acetylcysteine in the final week of ethanol ingestion significantly reduced lung edema during perfusion ex vivo. We conclude that ethanol ingestion in rats alters alveolar type II cell glutathione levels and function, thereby predisposing the lung to acute edematous injury after endotoxemia. We speculate that chronic alcohol abuse in humans predisposes to ARDS through similar mechanisms.

Acetylcysteine↗