We conducted a population-based survey of respiratory diseases and lung function in a New Mexico Hispanic community, and developed spirometric prediction equations based on data from 576 children and adults. Spirometric test procedures were followed as recommended by the American Thoracic Society. For children 6 through 18 yr of age, we used a logarithmic model to predict spirometric parameters. We used simple linear regression for adults 25 through 80 yr of age. On the basis of exploratory analyses, we excluded adult subjects who were obese, defined as a body mass index of 30 kg/m2 or greater. This report describes these regressions. We did not perform regression analysis for those subjects between 19 and 24 yr of age because of small numbers and the inappropriateness of grouping these subjects with older adults for regression analysis. As an alternative to a regression equation for this age group specifically, we propose linear interpolation between values obtained using prediction equations developed for children and for adults. Finally, we compared the percent predicted values obtained from our internal prediction equations with equations from other populations of white children and adults. In general, the comparison equations underestimated the percent predicted values in our population.
Familial aggregation of ventilatory function has been described in several populations, but the effects of age and cigarette smoking on the extent of aggregation have not been well characterized. We used data from a survey of a Hispanic population in New Mexico to obtain estimates of heritability for FVC and FEV1 as percentages of predicted value. Product-moment correlations for FVC of spouse pairs were 0.18 (n = 90 pairs) if neither smoked, 0.013 (n = 45 pairs) if only the wife smoked, 0.18 (n = 118 pairs) if only the husband smoked, and -0.04 (n = 83 pairs) if both smoked. Correlations for FEV1 of spouse pairs were similar. Because parent-child correlations did not vary with sex, we calculated product-moment correlations from the pooled data. The parent-child correlations for nonsmoking parents with nonsmoking children 6 to 17 yr of age and living in the same house were 0.16 (n = 335 pairs) and 0.17 for FVC and FEV1, respectively. For parents whose children were 25 yr of age or older, the parent-child correlations for those living in different houses were 0.37 (n = 63 pairs) for FVC and 0.40 for FEV1 if neither smoked, and 0.24 (n = 27 pairs) for FVC and 0.14 for FEV1 if both smoked. Heritability estimates, estimated by path analysis, were 0.43 for FVC and 0.42 for FEV1 if neither family member smoked and 0.65 for FVC and 0.44 for FEV1 if both family members smoked. We conclude that there is a moderate degree of heritability of FVC and FEV1 with no substantial change based on age or smoking status.
In a population-based survey of respiratory disease in New Mexico Hispanics, we validated self-reports of cigarette use by 1,317 subjects against salivary cotinine level and end-tidal carbon monoxide concentration. For identifying likely deceivers about cigarette smoking among self-reported never smokers and former smokers, we used cutoff values of 20 ng/ml and 8 parts per million (ppm) for salivary cotinine and carbon monoxide, respectively. Among males and females, age-standardized prevalences of current smokers based upon questionnaire reports were 30.9 and 27.1%, respectively. After adjustment for cotinine alone, these percentages were 36.2 for males and 31.1 for females, and after adjustment for cotinine and carbon monoxide level, the corresponding percentages were 39.1 for males and 33.2 for females. We conclude that self-reports about smoking habits may lead to underestimation of the prevalence of current smokers and that questionnaire responses should be validated with biologic markers of tobacco smoke exposure.
We conducted a population-based household survey of respiratory disease in 2,029 children and adults and measured salivary cotinine levels by radioimmunoassay in 1,360 nonsmokers and ex-smokers. At all ages median and mean cotinine levels among nonsmokers and ex-smokers increased with the number of smokers in the home. The prevalence of a detectable level of cotinine was about 35% for those not living with a cigarette smoker and was greater with the number of cigarettes smoked by household members. In a multiple logistic regression model, the major determinants of a detectable level of cotinine in children were mother's smoking (odds ratio (OR) = 3.2), father's smoking (OR = 2.1), and smoking of other household members (OR = 4.0). Among adults, the effects of spouse's smoking were smaller with OR = 1.3 and 1.4 for husband's and wife's smoking, respectively. We conclude that in the general population cotinine can be frequently detected in the saliva of nonsmokers, even among those not living with a smoker.
Because Hispanics in the Southwest are genetically admixed with American Indians, the hypothesis has been advanced that the excess occurrence of diabetes mellitus, obesity, and gallbladder disease in this ethnic group may be genetic in origin and results from genes derived from American Indians. This report describes the prevalence of these diseases in 1,175 adult Hispanic participants in a survey of a New Mexico community conducted in 1984-1985. At nearly all ages, the majority of subjects had a body mass index of 25 kg/m2 or greater, and a substantial proportion exceeded 30 kg/m2. The prevalence of obesity was much greater in these Hispanics than is shown in nationwide data for US whites. Diabetes mellitus was also reported more often by Hispanic subjects in this survey than by US whites nationwide. A report of gallbladder trouble or of gallbladder removal was common in both males and females; the prevalence of gallbladder removal was as high in this population as in Mexican Americans previously studied in Starr County, Texas. In spite of the high prevalence of obesity, hypertension was less frequent among the New Mexico Hispanics than is shown in nationwide data for US whites. These findings complement those of previous surveys in Texas, which have shown a notably high proportion of adults to be obese, to have non-insulin-dependent diabetes mellitus, and to have gallbladder disease. The similar epidemiology of these diseases in the Hispanics of New Mexico and the Mexican Americans of Texas supports the hypothesis that American Indian admixture underlies the development of these conditions in Hispanics throughout the Southwest.
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