Biomedical subjects

S T Weiss

Publications and source records attributed to S T Weiss.

At least 91 records · Page 5Linked to original sources

PubMed1999

The FEF25-75/FVC ratio is associated with methacholine airway responsiveness. The normative aging study.

Airway responsiveness is known to be partly explained by geometric and anatomic factors. This cross-sectional investigation was undertaken to determine whether FEF25-75/FVC as a surrogate measure of airway size relative to lung size is associated with airway responsiveness to methacholine. Posteroanterior chest radiographs and spirometry were performed on a group of 929 middle aged and older men from an ongoing longitudinal study, the Normative Aging Study, who returned for their regularly scheduled examination between 1984 and 1989. Subjects had a mean age of 60.5 +/- 7.7 yr. FEV1, FEF25-75, and FVC were taken from spirometric results and FEF25-75/FVC ratios were obtained. Main bronchus (MB) and tracheal (TR) diameters and lung area (LA) were obtained from chest radiographs, and ratios of MB/LA and TR/LA were calculated for each subject and compared with FEF25-75/ FVC as measures of airway size relative to lung size. In a multiple linear regression model adjusting for age, height, initial FEV1, smoking, eosinophil count, and IgE level, FEF25-75/FVC was significantly related to the degree of methacholine airway responsiveness as measured by Log10 dose response slope (beta = -0.37, p < 0.001). Controlling for the same variables, both MB/LA (beta = -149.07, p < 0.001) and TR/LA (beta = -125.87, p < 0.001) were significant predictors of the degree of bronchial responsiveness in separate regression models; however, their effects were greatly attenuated when FEF25-75/ FVC was present in the same model. Similar results were obtained after excluding subjects with FEV1/ FVC </= 0.70 and subjects who had any smoking history. We conclude that FEF25-75/FVC as a surrogate measure of airway size relative to lung size is significantly associated with airway responsiveness.

Adult↗

PubMed1999

Predictors of repeated wheeze in the first year of life: the relative roles of cockroach, birth weight, acute lower respiratory illness, and maternal smoking.

While more than 80% of childhood asthmatics are allergic to one or more inhaled allergens, the role of inhaled allergens in the induction of wheeze in the first year of life is unknown. In a prospective birth-cohort study of 499 children of asthmatic/allergic parents from metropolitan Boston, we examined home allergen concentrations measured within the first 3 mo of life as predictors of repeated wheeze episodes in the first year of life. In multivariate analyses adjusting for maternal asthma and dog in the home, predictors of two or more wheeze episodes in the first year of life included maternal smoking during pregnancy (relative risk [RR] = 1.83; 95% confidence limit [CL]: 1.12, 3.00), lower respiratory illness in the first year of life (croup, bronchitis, bronchiolitis, or pneumonia) (RR = 2.25; 95% CL:1.58, 3.19), low birthweight (RR = 1.28, 95% confidence interval [CI]: 1.04, 1.58 for an interquartile difference), and Bla g 1 or 2 (cockroach) allergen level in the family room > 0.05 U/g dust (RR = 1.76; 95% CL: 1.20, 2.57). Cockroach allergen in the family room and repeated wheeze remained significant after adjustment for socioeconomic factors including race and income (RR = 1.63; 95% CL: 1.05, 2.55). It is unknown whether the association between cockroach and repeated wheeze in infancy represents a cockroach-related increased risk of bronchial inflammation through nonallergenic or allergenic mechanisms.

Allergens↗

PubMed1999

Smoking and airway hyperresponsiveness especially in the presence of blood eosinophilia increase the risk to develop respiratory symptoms: a 25-year follow-up study in the general adult population.

Airway hyperresponsiveness (AHR) constitutes a risk for development of respiratory symptoms. We assessed whether blood eosinophilia (>/= 275 eosinophils/microliters), skin test positivity (sum score >/= 3) and cigarette smoking (never, ex-smoker, 1-14 cig/d, 15-24 cig/d, >/= 25 cig/d) at the first of two successive surveys are related to the development of respiratory symptoms (chronic cough or phlegm, bronchitis, persistent wheeze, dyspnea, and asthma) at the second survey, and whether these relations are the same in subjects with (PC10 </= 8 mg/ml histamine) and without AHR. We analyzed data of the longitudinal Vlagtwedde-Vlaardingen Study (1965 to 1990) using logistic regression analyses with paired observations, taking multiple measurements within a person into account. In total, 995 men and 792 women contributed 4,403 paired observations. Eosinophilia in hyperresponsive subjects significantly increased the risk to develop one or more respiratory symptoms (odds ratio [OR] = 3.67, 95% confidence interval [CI] = 1.79 to 7.52), wheeze (OR = 5. 06, 95% CI = 2.11 to 12.13), and dyspnea (OR = 2.73, 95% CI = 1.13 to 6.60), independent of smoking, age, sex, area of residence, and time between two successive surveys. Smoking at the first of two successive surveys increased the risk to develop symptoms in a dose-dependent relation. Subjects with positive skin tests in the past were less likely to develop one or more respiratory symptoms (OR = 0.64, 95% CI = 0.46 to 0.88) and chronic phlegm (OR = 0.65, 95% CI = 0.42 to 1.00), independent of AHR. This longitudinal study in the general adult population shows that cigarette smoking and hyperresponsive subjects are at increased risk to develop respiratory symptoms, and especially so when eosinophilia is present in hyperresponsive persons.

Adolescent↗

PubMed1999

Association between a sequence variant in the IL-4 gene promoter and FEV(1) in asthma.

Recent family-based studies have revealed evidence for linkage of human chromosome 5q31 to the diagnosis of asthma, elevated serum IgE levels, and bronchial hyperresponsiveness. Among the candidate genes in this region is the gene encoding for human interleukin-4 (IL-4). We reasoned that this gene could also serve as a candidate gene with respect to asthma severity as indicated by the FEV(1) measured when bronchodilator treatment was withheld. To test this hypothesis, we examined a large population of patients with asthma (ascertained without respect to genetic characteristics), for associations between a genetic variant in the IL-4 promoter region (C-589T) and asthma severity, as indicated by FEV(1). We used amplification by the polymerase chain reaction followed by BsmF1 restriction digestion to assign genotypes at the IL-4 promoter C-589T locus. We compared genotypes at this locus in 772 Caucasian and African American patients with asthma of varying severity, and we used multiple regression analysis to relate genotypic findings to FEV(1). Among white individuals, the homozygous presence of the C-589T IL-4 promoter genotype (TT) was associated with a FEV(1) below 50% of predicted (p = 0.013; OR, 1.44; 95% CI: 1.09 to 1.90). Subjects with the TT genotype had mean FEV(1) (% predicted) values 4.5% lower than those of subjects with the wild-type (CC) genotype at this locus. FEV(1) values of white patients with a CC or CT genotype were broadly distributed, whereas the TT genotype was associated with a narrow distribution of low FEV(1) values. The frequency of the T allele was significantly greater (p = 1 x 10(-)(23)) among African American asthmatics (0.544) than among white asthmatics (0.183). These data provide the first evidence associating FEV(1) in patients with asthma and genetic determinants at any locus. Our data are consistent with the idea that the FEV(1) in asthma is the result of multiple factors; one of these factors is the genotype at the IL-4 C-589T locus. This locus is associated with a small but significant decrement in pulmonary function among white asthmatic subjects.

Adult↗

PubMed1999

Asthma attacks with eosinophilia predict mortality from chronic obstructive pulmonary disease in a general population sample.

We studied the association between allergy defined as eosinophilia (>/= 275 cells/mm(3)) and/or positive skin tests (sum score >/= 3) and mortality from chronic obstructive pulmonary disease (COPD) after adjustment for major risk factors. In addition, we investigated this association in subgroups of respiratory symptoms and lung function. We used data from 7,556 participants of the respiratory surveys in 1964 -1972 in the general populations of Vlagtwedde, Vlaardingen, and Meppel (The Netherlands; mean age +/- SD: 39.3 yr +/- 14 in the 1960s). In 1995, the vital status was available (5,135 alive, 106 lost to follow-up, 121 primary deaths from COPD, and 2,194 other primary causes of which 137 had a secondary death cause from COPD. Positive skin tests were not associated with increased COPD mortality. The association between eosinophilia and COPD mortality was restricted to those who had reported asthma attacks and was present for both COPD as a primary cause (relative risk [RR] = 4.80; 95% confidence interval [CI] 1.9 to 11.9) and combined primary and secondary causes of death (RR = 3. 90; 95% CI 2.05 to 7.40). We conclude that eosinophilia with asthma attacks is a risk factor for COPD mortality in addition to known risk factors also found in our study such as male gender, older age, current smoking, low lung function, underweight, and dyspnea.

Adolescent↗

PubMed1999

Eotaxin and impaired lung function in asthma.

We performed an association study of plasma eotaxin levels, eosinophil counts, total IgE levels, asthma diagnosis, and lung function in an ethnically diverse and geographically dispersed population. We studied 515 asthmatic and 519 normal subjects, none of whom was taking inhaled or oral corticosteroids. Logistic regression analysis demonstrated a direct relationship between asthma diagnosis and eotaxin levels (p < 0.0001). The odds of an asthma diagnosis increased with eotaxin quartile, with the highest quartile having an odds ratio of 5.4 (95% CI 3.2 to 9.2, p < 0.001) compared with the lowest eotaxin quartile. Eotaxin levels were inversely related to lung function (p < 0.001), with the mean percent predicted FEV(1) in the highest eotaxin quartile being 13.5 percentage points (SEM 2.1, p < 0.001) less than that in the lowest quartile. Plasma eotaxin levels were associated with asthma and inversely related to lung function independent of age, race, sex, or smoking status. When combined with eosinophil counts and IgE levels, eotaxin levels contributed to the odds of an asthma diagnosis and of impaired lung function. Our results are the first to associate eotaxin levels with asthma diagnosis and compromised lung function in a large geographically and ethnically diverse population.

Adult↗

PubMed1999

Familial aggregation of pulmonary function in a rural Chinese community.

We investigated familial aggregation of pulmonary function among asthma index families and randomly selected nuclear families in a rural community in China. Measurements of pulmonary function and related risk factors were obtained from each family member. A generalized estimation equation model was used to explore the independent relation of pulmonary function among family members, with adjustment for sex, age, height, weight, education, smoking, and asthma status. There was a significant parent-child and sib-sib correlation of pulmonary function. The parent-child correlation of pulmonary function was similar for the first and second children. The correlation was greatest between sib-sibs, followed by mother-child, and less pronounced between father-child among asthma families. The rate of reduced pulmonary function in a subsequent sibling was lowest (4.0%) when both of the parents and the first sibling were in the high-pulmonary-function tertile (high-high group) and was highest (18.4%) when both the parents and the first sibling were in the low-pulmonary-function tertile (low-low group). The rates were intermediate if only the parents (7.0%, low-high group) or only the first sibling (11.5%, high-low group) was in the reduced-pulmonary-function tertile. Our data indicate a strong familial aggregation of pulmonary function in both asthma and random families in this population.

Adolescent↗

PubMed1999

Bronchodilator responsiveness and serum total IgE levels in families of probands with severe early-onset COPD.

Bronchodilator responsiveness has been associated with a subsequent accelerated decline in forced expiratory volume in one second (FEV1). Therefore, bronchodilator responsiveness and total serum immunoglobulin E(IgE) levels were assessed in 184 adult first-degree relatives of probands with severe early-onset chronic obstructive pulmonary disease (COPD) and a control group. Greater bronchodilator responsiveness was found among current smokers or exsmokers who were first-degree relatives of early-onset COPD probands than in currently or exsmoking controls, expressed as increase in FEV1 as a percentage of baseline (5.8+/-8.1 versus 2.9+/-5.1%, p<0.01), absolute increase in FEV1 from baseline (120+/-130 versus 60+/-110 mL, p<0.05), and increase in FEV1 as a percentage of the predicted value (3.6:4.1 versus 2.2+/-3.9%, p<0.05). However, elevated total serum IgE levels were not found in first-degree relatives of early-onset COPD probands compared with control subjects. The increased bronchodilator responsiveness among currently smoking/exsmoking first-degree relatives of early-onset COPD probands suggests that these individuals may have enhanced susceptibility to the detrimental effects of cigarette smoking.

Adult↗

PubMed1999

Environmental tobacco smoke exposure and asthma in adults.

Environmental tobacco smoke (ETS) contaminates indoor air in homes and workplaces. Although the adverse effects of active cigarette smoking on the respiratory tract have been extensively characterized, the effects of ETS exposure on adult asthma have not yet been investigated extensively and the available data are limited. This article examines the evidence for ETS exposure as a cause of asthma and asthma exacerbation in adults, and for ETS exposure in the workplace specifically as contributing to these health effects. It addresses methodological barriers that limit the available data and evaluates the adequacy of the data for risk assessment.

Adult↗

PubMed1999

Day care attendance in the first year of life and illnesses of the upper and lower respiratory tract in children with a familial history of atopy.

OBJECTIVE: To examine the relationship between day care attendance and illnesses of the upper and lower respiratory tract in the first year of life. STUDY DESIGN: Prospective birth cohort study. METHODS: Children (N = 498) who had at least 1 parent with a history of allergy or asthma were enrolled at birth and followed prospectively for the first year of life. A home visit at 2 to 3 months of age and bimonthly telephone questionnaires were used to obtain information on day care arrangements, home characteristics, respiratory symptoms, and physician-diagnosed illnesses of the upper and lower respiratory tract. RESULTS: Day care attendance in the first year of life was associated with two or more doctor-diagnosed ear infections (OR: 2.4; 95% CI: 1.7-3.6), three or more parental reports of runny or stuffed nose (OR: 3.2; 95% CI: 1.9-5.5), a doctor's diagnosis of sinusitis (OR: 2.2; 95% CI: 1.1-4.2), and doctor-diagnosed lower respiratory illnesses (croup, bronchitis, bronchiolitis, and pneumonia; OR: 1.6; 95% CI: 1.0-2.4). For children attending day care, exposure to pets in day care, the presence of a rug or carpet in the area where the child slept in day care, and a nonresidential setting for day care all were independent predictors of two or more doctor-diagnosed ear infections. CONCLUSIONS: The results suggest that day care increases the risk of illnesses of the upper and lower respiratory tract in the first year of life for children with a familial history of atopy. Specific environmental exposures within day care, such as the presence of pets or having a rug or carpet in the area where children sleep, may increase the risk of recurrent ear infections in the first year of life among children with familial history of atopy who attend day care.

Asthma↗

PubMed1998

Electrocardiographic conduction disturbances in association with low-level lead exposure (the Normative Aging Study).

Recent research indicates that cumulative exposure to lead may be more toxic than previously thought. This study was undertaken to examine the relation of low-level lead exposure to electrocardiographic (ECG) conduction disturbances among 775 men who participated in the Normative Aging Study (average age 68 years; range 48 to 93). We used K-x-ray fluorescence to measure lead levels in the tibia and patella, and graphite furnace atomic absorption spectroscopy to measure blood lead levels. The mean (SD) values for blood lead, tibia lead, and patella lead were 5.8 (3.4) microg/dl, 22.2 (13.4) microg/g, and 30.8 (19.2) microg/g, respectively. Bone lead levels were found to be positively associated with heart rate-corrected QT and QRS intervals, especially in younger men. Specifically, in men <65 years of age, a 10 microg/g increase in tibia lead was associated with an increase in the QT interval of 5.03 ms (95% confidence interval [CI], 0.83 to 9.22) and with an increase in the QRS interval of 4.83 ms (95% CI, 1.83 to 7.83) in multivariate regression models. In addition, an elevated bone lead level was found to be positively associated with an increased risk of intraventricular block in men <65 years of age and with an increased risk of atrioventricular (AV) block in men > or = 65 years of age. After adjustment for age and for serum high-density lipoprotein (HDL) level, a 10 microg/g increase in tibia lead was associated with an odds ratio (OR) of 2.23 (95% CI, 1.28 to 3.90) for intraventricular block in men <65 years of age and with an OR of 1.22 (95% CI, 1.02 to 1.47) for AV block in men > or = 65 years of age. Blood lead level was not associated with any of the ECG outcomes examined. The results suggest that cumulative exposure to lead, even at low levels, may depress cardiac conduction.

Aged↗

PubMed1998

Prospective study of a self-report type A scale and risk of coronary heart disease: test of the MMPI-2 type A scale.

BACKGROUND: Several methods exist by which to assess type A behavior (TAB). Although the videotaped clinical interview is regarded as the "gold standard," self-report measures have also proved useful in assessing TAB in large population studies. The purpose of this study was to examine prospectively the relationship of TAB to risk of coronary heart disease (CHD) incidence with the use of the revised Minnesota Multiphasic Personality Inventory (MMPI-2) Type A Scale. To the best of our knowledge, this is the first test of this scale in the context of predicting CHD incidence. METHODS AND RESULTS: The study was performed in the VA Normative Aging Study, an ongoing cohort of older (mean age, 61 years) community-dwelling men. A total of 1305 men who were free of diagnosed CHD in 1986 completed the MMPI-2 Type A Scale. During an average 7.0 years of follow-up, 110 cases of incident CHD occurred. Compared with men in the lowest quartile of type A scores, men in the highest quartile had multivariate adjusted relative risks of 2.86 (95% CI, 1.19 to 6.89; P for trend=0.016) for combined CHD death and nonfatal myocardial infarction (MI) and 2.30 (95% CI, 1.32 to 4.01; P for trend=0.001) for combined CHD death/nonfatal MI plus angina pectoris. The relationship of TAB to CHD was independent of measures of anger and cynicism. CONCLUSIONS: The MMPI-2 Type A Scale predicts CHD incidence. Further research is warranted to examine the correlation, if any, between this scale and the videotaped clinical interview.

Adult↗

PubMed1998

Anxiety and coronary heart disease: a synthesis of epidemiological, psychological, and experimental evidence.

The purpose of this review is to examine the epidemiological, psychological, and experimental evidence for an association between anxiety and coronary heart disease (CHD). Papers published during the years 1980-1996 on anxiety and CHD and relevant publications from earlier years were selected for this review. Epidemiologic evidence suggests that anxiety may be a risk factor for the development of CHD. Chronic anxiety may increase the risk of CHD by: (a) influencing health behaviors (e.g. smoking); (b) promoting atherogenesis (e.g. via increased risk of hypertension); and (c) triggering fatal coronary events, either through arrhythmia, plaque rupture, coronary vasospasm, or thrombosis. Electrophysiologic evidence is particularly compelling: anxiety appears to be associated with abnormal cardiac autonomic control, which may indicate increased risk of fatal ventricular arrhythmias. The strength, consistency, and dose-response gradient of the association between anxiety and CHD, together with the biologic plausibility of the experimental evidence, suggest that anxiety may contribute to risk of CHD and that the relationship warrants further investigation.

Anxiety Disorders↗

PubMed1998

Indoor allergens and longitudinal FEV1 decline in older adults: the Normative Aging Study.

We investigated the relationship between home allergen exposure and decline in FEV1 in 10 asthmatic and 30 randomly selected, age-matched, nonasthmatic participants in the Normative Aging Study. We defined asthma as subject-reported wheezing apart from colds, with either a physician's diagnosis of asthma or a methacholine PD20 FEV1 of 8.6 micromol or less. We examined the relationship between the annual decline in FEV1 and the concentrations of the cockroach (Blattella germanica) allergens Bla g 1 and Bla g 2, the dust mite (Dermatophagoides pteronyssinus and Dermatophagoides farinae) allergens Der p 1 and Der f 1, and the cat (Felis domesticus) allergen Fel d 1 in house dust specimens. Bla g 1 (-79.8 ml/yr, p = 0.0006) and Bla g 2 (-40.81 ml/yr, p = 0.0004) were significant predictors of decline in FEV1 after adjustment for age, smoking, and baseline FEV1. These results were unchanged after elimination of the asthmatic subjects from the analysis. We conclude that cockroach allergen levels in homes is a risk factor for accelerated decline in FEV1 independent of airway responsiveness.

Adult↗

PubMed1998

Blood pressure at age 3-24 years in a rural community in Anhui, China.

PURPOSE: This community-based study in Anhui, China examined the sex-specific pattern of blood pressure (BP) and its major determinants between age 3 and 24 years. METHODS: BP, height, weight, and related covariates were obtained from all eligible subjects by consistent methods. A generalized additive model was used to explore independent relations between BP and covariates. The sample for analyses included a total of 14,277 subjects (7244 males and 7033 females). RESULTS: Systolic blood pressure (SBP) increased linearly with age to an apparent plateau around the age of 15 years in girls and 20 years in boys. Diastolic blood pressure (DBP) essentially paralleled SBP. Until the age of 10, both SBP and DBP were similar in boys and girls; thereafter, values for boys surpassed those for girls with an average difference of 9 mmHg and 4 mmHg for SBP and DBP, respectively, at 20 years of age. This sex difference appeared to persist into early adulthood. The independent relation between BP and each of the three major determinants (age, height, and weight) was nonlinear over the age range studied. Sex-specific regression models with linear terms for age, height and weight were developed for each of four age groups (3-9, 10-14, 15-19, 20-24 years). The 5th, 10th, 90th, and 95th percentiles based on the percentage of predicted values can serve as the cutoffs for low, normal-low, normal-high, and high BP. The predicted values were derived from the above regression models that take into account an individual's sex, age, height, and weight. CONCLUSIONS: This analysis provided important basis for classification of hypertension status and subsequent investigation of environmental risk factors in this population.

Adolescent↗

PubMed1998

Environmental risk factors in childhood asthma.

Eighty per cent of all childhood asthma has its onset by 3 years of age. A similar percentage of childhood asthma is associated with atopy (presence of allergic rhinitis or eczema and/or positive skin prick tests). Defined risk factors for childhood asthma include allergen exposure, environmental tobacco smoke, viral respiratory illness, the presence of other atopic disease, and gender. Although a large percentage of children will have remission of asthma as they grow, they will retain the intermediate phenotypes of increased airway responsiveness and allergen and, therefore, be at risk of recrudescence of disease in adult life.

Allergens↗

PubMed1998

Limitations of a home characteristics questionnaire as a predictor of indoor allergen levels.

We examined associations between reported home characteristics and levels of indoor allergens in 499 homes of a birth cohort of children of allergic/asthmatic families from the Boston area. The risk of having dust mite allergen (Der f 1 or Der p 1) > or = 2 microg/g on the bedroom floor was highest in houses, but 16% of apartments had levels this high. Compared with that from smooth floors, dust from carpeted bedroom floors had 2.1 times the risk of dust mite allergen > or = 10 microg/g, but levels exceeded 2 microg/g in 32% of uncarpeted floors. The risk of dust mite allergen > or = 10 microg/g of dust from plastic-encased mattresses was 0.5 times that for cloth mattresses, but levels in 21% of plastic-encased mattresses were > or = 2 microg/g. In 93% of homes with and 3% of homes without cats, Fel d 1 was > or = 8 microg/g, but 34% of homes without cats had Fed d 1 > or = 1 microg/g. Cockroach allergen (Bla g 1 or Bla g 2) was > or = 2 U/g of kitchen dust in 26% of apartments and only 6% of houses, and it was detected in 48% of homes with no reported signs of cockroaches in the previous 12 mo. Home characteristics reporting is a relatively weak predictor of the absence of allergen, and exposure can occur even when no cats are present, beds are encased in plastic, no carpets are present, and no signs of cockroaches have been reported.

Air Pollution, Indoor↗

PubMed1998

Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis.

Severe alpha-1-antitrypsin deficiency is the only proven genetic risk factor for chronic obstructive pulmonary disease (COPD). We have assembled a cohort of 44 probands with severe, early-onset COPD, who do not have severe alpha-1-antitrypsin deficiency. A surprisingly high prevalence of females (79.6%) was found. Assessment of the risk to relatives of these early-onset COPD probands for airflow obstruction and chronic bronchitis was performed to determine whether significant familial aggregation for COPD, independent of alpha-1-antitrypsin deficiency, could be demonstrated. First- degree relatives of early-onset COPD probands had significantly lower FEV1 and FEV1/FVC values than control subjects (p < 0.01), despite similar pack-years of smoking. Reduced spirometric values in first-degree relatives of early-onset COPD probands were found only in current or ex-cigarette smokers. The mean FEV1 in current or ex-smoking first-degree relatives was 76.1 +/- 20.9% predicted compared to 89.2 +/- 14.4% predicted in current or ex-smoking control subjects (p < 0.01); in lifelong nonsmokers, the mean FEV1 was 93.4% predicted for both control subjects and first-degree relatives of early-onset COPD probands. Generalized estimating equations, adjusting for age and pack-years of smoking, demonstrated increased odds of reduced FEV1 and chronic bronchitis in current or ex-smoking first-degree relatives of early-onset COPD probands. Using a new method to estimate relative risk from relative odds, we estimate that the relative risks for FEV1 below 60%, FEV1 below 80%, and chronic bronchitis are each approximately three in current or ex-smoking first-degree relatives of early-onset COPD probands. The increased risk to relatives of early-onset COPD probands for reduced FEV1 and chronic bronchitis, limited to current or ex-smokers, suggests genetic risk factor(s) for COPD that are expressed in response to cigarette smoking.

Bronchitis↗