The Big Breakfast Study: Chrono-nutrition influence on energy expenditure and bodyweight.

A growing body of evidence highlights the importance of the biological clock as a modulator of energy balance and metabolism. Recent studies in humans have shown that ingested calories are apparently utilised more efficiently in the morning than in the evening and this is manifest through improved weight loss, even under iso-energetic calorie intake. The mechanisms behind this enhanced morning energy metabolism are not yet clear, although it may result from behavioural adaptations or circadian driven variations in physiology and energy metabolism. A major objective of the newly funded Big Breakfast Study therefore is to investigate the mechanistic basis of this amplified morning thermogenesis leading to enhanced weight loss, by exploring behavioural and physiological adaptations in energy expenditure alongside the underlying circadian biology. This report briefly discusses the current research linking meal timing, circadian rhythms and metabolism; highlights the research gaps; and provides an overview of the studies being undertaken as part of the Medical Research Council-funded Big Breakfast Study.

Pathologic features and molecular phenotype by patient age in a large cohort of young women with breast cancer.

Prior studies have suggested a higher prevalence of high grade, ER-negative, HER2-positive, and basal-like carcinomas in young women with breast cancer. However, the precise distribution of poor prognostic features in this population remains unclear. We examined the pathologic features and distribution of molecular phenotype in relation to patient age in a large group of young women (≤40 years) with invasive breast cancer. Medical records were reviewed for clinical characteristics, tumor stage, and receptor status. Pathologic features, including those features associated with basal-like carcinomas, were examined by central review. Using tumor grade and biomarker expression, cancers were categorized as luminal A (ER+ and/or PR+ and HER2-, histologic grade 1 or 2); luminal B (ER+ and/or PR+ and HER2+, or ER and/or PR+, HER2- and grade 3); HER2 (ER and PR- and HER2+); and triple negative (ER-, PR-, and HER2-). Among 399 women of ≤40 years, 33% had luminal A tumors, 35% luminal B, 11% HER2 (ER-negative), and 21% triple negative. Compared to published results for all breast cancers, a greater proportion of young women had luminal B tumors, and a lesser proportion had luminal A. There were no significant differences in molecular phenotype, tumor stage or grade among the different age groups of young women. However, this population of young women presented with a different distribution of molecular phenotypes compared to the general population of women with breast cancer. These findings may have implications with regard to the etiology and prognosis of breast cancer in young women.

Papillary lesions of the breast: selected diagnostic and management issues.

The assessment and categorization of papillary lesions remains one of the most challenging areas in breast pathology. In this review, we will focus on several diagnostic and management issues related to papillary breast lesions that are frequently encountered in daily practice. These include: (i) the distinctions among papillomas with atypia (atypical papillomas), papillomas with ductal carcinoma in situ, and papillary ductal carcinoma in situ; (ii) recent developments in our understanding of encapsulated ('intracystic') papillary carcinomas and solid papillary carcinomas; and (iii) the impact of core needle biopsy on management decisions and specimen evaluation. The role of immunohistochemistry in the evaluation of these lesions, particularly the role of myoepithelial cell markers, will be emphasized.

Relative risk of high grade squamous intraepithelial lesion associated with prior abnormal Pap smears.

OBJECTIVE: Pap smear frequency remains controversial, especially for women with consecutive negative smears. We undertook the current study to ascertain the association of high grade squamous intraepithelial lesions (HSIL) and prior abnormal Paps. STUDY DESIGN: Women with biopsy-proven HSIL (cervical intraepithelial neoplasia 2 and 3) diagnosed between September 1996 and December 1997 and age-matched controls with a negative Pap obtained during the same time period were selected. RESULTS: Sixty-three cases (mean age = 32 years) of HSIL and 69 controls (mean age = 33 years) constituted the study population. Any prior abnormal diagnosis conferred a 15-fold increased risk of HSIL on the current Pap (50/63 vs. 14/69, P < .0001). When limited to the 60 women with at least three prior Paps, the odds ratio for HSIL on the current Pap with any prior abnormal was 18 (28/31 vs. 10/29, P < .0001). Three cases had at least three consecutive negative Paps prior to the diagnosis of HSIL. CONCLUSION: Women with one or more prior negative Pap smears had a significantly decreased risk of HSIL on the current Pap. Consecutive negative Paps did not appear to further decrease the risk; 10% of HSIL patients had had three or more consecutive prior negative Paps. To detect HSIL at its earliest stage, women should be advised to continue annual Pap screening in spite of consecutive negative results.

Excitatory lung reflex may stress inspiratory muscle by suppressing expiratory muscle activity.

Recently, a vagally mediated excitatory lung reflex (ELR) causing neural hyperpnea and tachypnea was identified. Because ventilation is regulated through both inspiratory and expiratory processes, we investigated the effects of the ELR on these two processes simultaneously. In anesthetized, open-chest, and artificially ventilated rabbits, we recorded phrenic nerve activity and abdominal muscle activity to assess the breathing pattern when the ELR was evoked by directly injecting hypertonic saline (8.1%, 0.1 ml) into lung parenchyma. Activation of the ELR stimulated inspiratory activity, which was exhibited by increasing amplitude, burst rate, and duty cycle of the phrenic activity (by 22 +/- 4, 33 +/- 9, and 57 +/- 11%, respectively; n = 13; P < 0.001), but suppressed expiratory muscle activity. The expiratory muscle became silent in most cases. On average, the amplitude of expiratory muscle activity decreased by 88 +/- 5% (P < 0.002). The suppression reached the peak at 6.9 +/- 1 s and lasted for 200 s (median). Injection of H(2)O(2) into the lung parenchyma produced similar responses. By suppressing expiration, the ELR produces a shift in the workload from expiratory muscle to inspiratory muscle. Therefore, we conclude that the ELR may contribute to inspiratory muscle fatigue, not only by directly increasing the inspiratory activity but also by suppressing expiratory activity.

Pulmonary rapidly adapting receptor stimulation does not increase airway resistance in anesthetized rabbits.

In open-chest artificially ventilated rabbits, removal followed by replacement of positive end-expiratory pressure (PEEP maneuver) favors stimulation of airway rapidly adapting receptors (RARs). The purpose of the present study was to determine whether activation of RARs can cause bronchoconstriction. We measured airway pressure, airflow, and tidal volume, and calculated dynamic lung compliance and total lung resistance. PEEP maneuver increased airway pressure swings (16.4 +/- 4% above control; p = 0.0016) and decreased compliance (to 84.8 +/- 2.8% of control; p = 0.0002) without changing resistance (108.0 +/- 4.4% of control; p = 0.85). On the other hand, the resistance increased greatly (93 +/- 13%, p < 0.01) after intravenous injection of acetylcholine or electrical stimulation of vagal efferents, indicating that our system could detect increases in the resistance. In a separate group, we stimulated RARs by stroking the trachea with a cotton tip (tickling), tickling produced cough, manifested by increased pressure and flow without resistance changing. These changes were abolished after paralysis with succinylcholine. Because we did not detect an increase in airflow resistance during activation of RARs by the PEEP maneuver and tickling, we conclude that increase in resistance may not be an important reflex component of airway RARs.

The effect of smoking on energy expenditure and plasma catecholamine and nicotine levels during light physical activity.

A number of studies have found that cigarette smoking causes an acute increase in resting energy expenditure, but the effect on energy expenditure during light physical activity is less clear. Since both smoking and activity have been shown to increase plasma catecholamines, these could produce additive effects on energy expenditure when smoking during light physical activity. In this study, the impact of cigarette smoking on energy expenditure, cardiovascular function, plasma nicotine and plasma catecholamine levels was determined in adult male subjects at rest and while engaged in light physical activity. Smoking at rest resulted in a 3.6% increase in energy expenditure above the resting baseline; whereas the increase in energy expenditure caused by smoking during light physical activity (compared with the light physical activity baseline) was 6.3%. This increase during light physical activity was significantly greater than the increase observed at rest (p < 0.025). As expected, plasma nicotine increased with smoking during both rest and light physical activity. An increase in plasma nicotine was associated with smoking during light physical activity. When this increase was adjusted as a covariate, the difference in smoking-related energy expenditure between light physical activity and rest disappeared, suggesting nicotine accounts for the effect. Plasma epinephrine and norepinephrine levels increased with smoking and showed a significantly greater increase during light physical activity compared to rest. Cigarette smoking caused a significantly greater increase in heart rate during light physical activity than it did while at rest, but there was no significant effect of smoking on mean blood pressure. It was concluded that there is enhanced energy expenditure associated with cigarette smoking during light physical activity when compared with smoking at rest which could be due in part to smoking-induced increases in circulating plasma catecholamines and perhaps nicotine.

Effects of platelet-activating factor on arteriolar and venular tone in rat trachea.

Platelet-activating factor (PAF) causes altered vascular tone in the mesenteric, pulmonary, and skeletal muscle vascular beds, enhanced macromolecular leak in postcapillary venules, and bronchoconstriction. In spontaneously breathing, anesthetized male Sprague-Dawley rats, we examined responses of individual tracheal microvessels using intravital video microscopy with epi-illumination using a polarizing filter and a long working distance lens (10x). Topical application of PAF (0.1 ml; 10(-9), 10(-7), or 10(-5) M) caused venules (diameter, 51 +/- 5 microm, mean +/- SEM) to constrict in a concentration-dependent fashion. Venoconstriction began within 0-3 min and was maximal within 10 min. In contrast, PAF (10(-5) M) applied to arterioles (diameters, 37 +/- 1 microm) ultimately caused constriction by 21 +/- 7%, but in three dilation (38 +/- 9%) occurred first. PAF (10(-7) and 10(-9) M) applied to arterioles (diameter 36 +/- 3 and 38 +/- 3 microm, respectively) caused no significant change in diameter. Infusion of BN52021, a PAF receptor antagonist, completely blocked constriction of venules and arterioles to PAF (10(-5) M), but dilation (17 +/- 0.2%) still occurred in three of five arterioles. Infusion of Nomega-nitro-l-arginine methyl ester (L-NAME; 1 mg/kg/min), a nitric oxide (NO) synthase inhibitor, potentiated venoconstriction by 34 +/- 18% in response to PAF (10(-7) M) and blocked arteriolar dilation to PAF (10(-5) M). Arteriolar constriction was unaffected by inhibiting NO release. Topical application of L-NAME (10(-3) M) constricted venules (n = 6) by 13 +/- 2% and arterioles (n = 5) by 26 +/- 4%. Venules constricted 33 +/- 15% less to PAF (10(-7) M, n = 5) following topical L-NAME (33 +/- 15%) than with infused l-NAME. Arterioles (n = 5) constricted 27 +/- 4% to PAF (10(-5) M) after topical l-NAME, no different from the group receiving infused L-NAME. We conclude that (1) PAF has a greater vasoconstrictive effect on tracheal venules than arterioles; (2) arterioles have a biphasic response to PAF at some concentrations; (3) PAF-induced vasoconstriction, but not dilation, is receptor mediated; (4) nitric oxide attenuates tracheal venoconstriction and may cause arteriolar dilation in response to PAF; and (5) endogenous release of NO appears to modulate the basal tone of tracheal arterioles more than venules.

Direct effects of meconium on rat tracheal smooth muscle tension in vitro.

Increased airway resistance is a component of the meconium aspiration syndrome. Experiments were done to determine whether meconium can have a direct affect on tracheal smooth muscle tension. Tracheal segments (4-5 mm long) were isolated from male Sprague-Dawley rats and suspended in organ baths with physiologic salt solution at 37 degrees C gassed with 95% O2-5% CO2. Each segment was attached to a fixed glass rod on one side and to a force displacement transducer on the other side to measure transverse tension. The segments were stretched to 1.5 g of tension and equilibrated for 2-5 h. Human meconium was diluted in physiologic salt solution (20 g/100 mL) and filtered through gauze. Tension was generated in the segments by adding acetylcholine (10(-6) M) to the tissue bath. Addition of meconium to the organ bath (0.1-5 mg/mL) caused tracheal smooth muscle relaxation in 44% of tracheal segments tested. Contraction occurred in 8% of tested segments, but only at the intermediate and low doses. The amount of relaxation increased significantly in a concentration-dependent manner. These responses were not affected by pretreating segments with indomethacin, removing the tracheal epithelium, using KCl to generate tone, or by heating meconium above 60 degrees C for 1 h. Addition of oleic acid to the organ bath (3.5 x 10(-6) to 3.5 x 10(-4) M) caused concentration-dependent tracheal smooth muscle responses (with relaxation predominating at 3.5 x 10(-4) M and contraction predominating at 3.5 x 10(-6) M). These results suggest that meconium can cause tracheal smooth muscle relaxation by a mechanism that does not appear to be mediated by cyclooxygenase products, by the tracheal epithelium, or a protein. The direct action of meconium on tracheal smooth muscle, which may in part be mediated by a fatty acid, does not appear to contribute significantly to the increased airway tone associated with the meconium aspiration syndrome.

Smoking multiple high- versus low-nicotine cigarettes: impact on resting energy expenditure.

The thermic effect of smoking multiple cigarettes varying substantially in nicotine yield was investigated. Three treatments were imposed: nonsmoking at baseline, smoking six low-nicotine (0.8 mg nicotine) cigarettes (LOW), and smoking six high-nicotine (1.74 mg nicotine) cigarettes (HIGH). An initial increase of 6.8% in resting energy expenditure (REE) above baseline REE occurred after consumption of two consecutive cigarettes for both the HIGH and LOW treatments. With consumption of more cigarettes, the peak increase for the HIGH treatment was 9.3%, significantly greater than the peak of 5.9% for the LOW. Averaged over 2 hours, the HIGH treatment significantly increased REE by 6.9% and the LOW treatment significantly increased REE by 5.2%. Expired carbon monoxide (CO) measurements indicated that LOW cigarettes were smoked more aggressively than HIGH cigarettes. It was concluded that, initially, the nicotine yield of cigarettes is not an important influence on the thermic effect of smoking. But over a longer period and after multiple cigarettes, the nicotine yield may become an important influential factor.

Qualifiers of atypical squamous cells of undetermined significance help in patient management.

According to the recommendations of the Bethesda System, the diagnosis of atypical squamous cells of undetermined significance (ASCUS) should be further qualified, when possible, as to whether a reactive or a squamous intraepithelial lesion (SIL) is favored. To determine the utility of this recently proposed terminology, we undertook this study to correlate the diagnosis of ASCUS (with or without qualifiers) with results obtained from examination of biopsy specimens. All patients were identified for the study who had a coloposcopically obtained cervical biopsy specimen or endocervical curettage specimen recorded in the surgical pathology files at Beth Israel Hospital, Boston, Massachusetts, from April 1994 through September 1994 and had either prior or concurrent Pap smear(s) reported as ASCUS, ASCUS-favor reactive, ASCUS-favor SIL, or SIL-low grade (SIL-LG). Patients with a cytologic diagnosis of SIL-LG served as a reference group. A total of 435 patients with 485 Pap smears were included. The prevalence rates of biopsy-proven SIL in patients with a cytologic diagnosis of ASCUS-favor reactive, ASCUS, ASCUS-favor SIL, and SIL-LG were 10, 28, 36, and 55%, respectively. The difference between cases diagnosed as ASCUS (with or without qualifiers) and SIL-LG, with respect to the presence of SIL at examination of the biopsy specimen, was statistically significant (P < 0.001 for all correlations). Cases diagnosed as ASCUS-favor reactive had a significantly lower rate of biopsy-proven SIL compared with those diagnosed as ASCUS and ASCUS-favor SIL (P < 0.01 for both correlations). A significant proportion of biopsy specimens with Pap smear diagnosis of ASCUS-favor SIL had SIL-high grade (15%). In contrast, an underlying SIL-high grade is much less likely in patients with ASCUS (unqualified) (3%) or when a reactive process is favored (3%). It seems justified to manage patients with ASCUS-favor SIL in a manner similar to those with SIL-LG. A conservative management seems appropriate for patients with ASCUS and ASCUS-favor reactive.

The effect of body fat distribution on pulmonary function tests.

Although the influence of obesity on pulmonary function tests has been examined, the role of body fat distribution has received limited attention. Pulmonary studies of patients severely affected by upper body obesity suggest they have more severely compromised lung volumes than obese patients with lower body obesity. We examined 42 healthy but normal or mildly obese men to determine if body fat distribution influences pulmonary function tests. Multiple measures of adiposity showed a significant inverse relationship with both spirometry and static lung volumes. However, the biceps skinfold thickness had the strongest inverse relationship with total lung capacity (TLC) compared to other anthropometric measures. The waist-to-hip ratio (WHR) demonstrated a significant inverse relationship with static lung volumes only when controlling for cigarette smoking. However, comparing pulmonary function tests between patients with a WHR less than 0.950 (lower body fat distribution) and subjects with a WHR of 0.950 or greater (upper body fat distribution) revealed that FVC, FEV1, and TLC were significantly lower in the patients with upper body fat distribution. Stepwise multiple regression analysis was done using all anthropometric variables and age which generated predictive equations that included the biceps skinfold thickness for residual volume (RV) and TLC. This suggests that upper body fat distribution may be associated with a modest impairment of lung volumes in normal and mildly obese men. Until the findings of this study can be applied to a larger, ethnically and anthropometrically diverse population, and to women, we believe caution is warranted when standard equations are used to predict pulmonary function tests in an anthropometrically diverse population.

Effect of caffeine and/or cigarette smoking on resting energy expenditure.

The thermic effect of cigarette smoking is dampened by the thermic effect of a meal, but potentiated by the thermic effect of exercise. The impact of the combined influences of caffeine and cigarette smoking is unknown. We examined the 3-h thermic response to smoking four 0.8 mg nicotine cigarettes, ingesting 200 mg of caffeine, or both, in ten fasted healthy men. Smoking four 0.8 mg nicotine cigarettes increased resting energy expenditure (REE) by 3.3% over a 3 h measurement period. Consumption of 200 mg of caffeine in the fasted condition increased REE of the smokers by 4.8% over 3 hours. Smoking four 0.8 mg cigarettes and ingesting 200 mg of caffeine significantly increased REE by 7.5% during the 3 h measurement period. At times early in the observation period, the combined thermic effect of cigarettes and caffeine was more than additive, but the effect was short-lived. A control group of nonsmokers was studied comparing REE following placebo or 200 mg of caffeine. Caffeine increased REE in the non-smoking controls 6.7%. This was not significantly different from results obtained on smokers. Fasted and non-smoking (baseline) REE was similar in smokers and non-smoking control subjects. It was concluded that the effects of caffeine on REE are additive.

High-resolution CT in simple coal workers' pneumoconiosis. Lack of correlation with pulmonary function tests and arterial blood gas values.

We examined 21 miners by means of standard chest radiography, high-resolution computerized tomography (HRCT), pulmonary function tests, and resting arterial blood gas levels. Using the ILO/UC classification of pneumoconiosis, 7 miners had category 1/0 or 2/1 simple coal workers' pneumoconiosis (CWP). By HRCT, nodules were identified in 12 miners; 4 of 9 were classified as category 0/0 CWP; 2 of 5, 0/1 CWP; 5 of 6, 1/0 CWP; and 1 of 1, 2/1 CWP by chest radiograph. Focal emphysema was identified by HRCT in 7 miners; 4 of 9 were classified as 0/0 CWP; 2 of 5, 0/1 CWP; and 1 of 6, 1/0 CWP by standard chest radiography. Four miners with definite nodules confirmed by HRCT had focal emphysema, while three without nodules had focal emphysema. Pulmonary function testing was not different between miners with or without CWP by standard chest radiography, nor was it different between miners with or without definite nodules evidenced by HRCT. No difference in resting oxygenation was found between any group of miners. The presence of focal emphysema confirmed by HRCT did not significantly affect pulmonary function tests on resting arterial blood gas values. There was, however, a significantly lower FEV1 and mean forced expiratory flow during the middle half of forced vital capacity with lifetime nonsmoking miners. The presence of CWP on chest radiography was significantly correlated with smoking cigarettes but not the years of mining. The presence of nodules on HRCT approached a significant correlation with cigarette smoking, but focal emphysema did not. For detecting evidence of coal dust accumulation in lung parenchyma and identifying focal emphysema, HRCT was more sensitive than standard chest radiography. However, despite earlier detection of parenchymal abnormalities, abnormal pulmonary function attributable to coal dust could not be identified.

Bronchospasm secondary to replacement estrogen therapy.

A postmenopausal woman with severe obstructive airways disease and bronchospasm developed increased airflow limitation with the reintroduction of estrogen therapy for osteoporosis. Discontinuation of the estrogen caused symptomatic improvement and decreased her corticosteroid requirement. Readministration of estrogen caused recrudescence of her symptoms and a decline in her peak expiratory flow rate and spirometric data, which reversed with withdrawal of the estrogen therapy. Bronchospasm during the luteal phase of the menstrual cycle is well known, but exacerbation of reactive airways disease with the administration of exogenous estrogen has not previously been reported; however, with the increasing practice of reintroducing estrogen in postmenopausal women to reduce the risk of symptomatic osteoporosis, other susceptible women may suffer clinically significant deterioration of their underlying pulmonary disease.

Juvenile laryngeal papillomatosis: a new complication.

Extension of juvenile papillomas to the lung parenchyma is unusual. When it occurs, the patient's prognosis worsens because these lesions destroy lung tissue as they grow. Respiratory complications eventually occur in the presence of multiple nodular and cystic lesions due to the attendant parenchymal destruction. We have observed that pneumothorax can occur after the development of cystic pneumatoceles, presumably from the ball valve effect of a nodular lesion (Fig 3).

Body fatness and smoking history predict the thermic effect of smoking in fasted men.

Epidemiological studies suggest that body composition and smoking history are related to degree of weight gain following smoking cessation. We hypothesized that body composition and smoking history affect the thermic effect of smoking (TES), which in turn would influence weight gain. Forty males ranging in age from 20 to 70 years smoked two cigarettes (0.8 mg nicotine yield) in 20 minutes, after which resting energy expenditure (REE) was measured during the next hour. The average change in REE (delta REE) was 4.97% (P < 0.0001), with a range of -2% to +14%. delta REE was greater than 1% in 35 subjects, less than 1% in three subjects, and reduced in two subjects. Body fatness was negatively correlated with delta REE (r = -0.68, r2 = 0.46). Multiple regression analysis indicated that body fatness (%) and pack-year history of smoking strongly predict delta REE (R = 0.82, R2 = 0.68; delta REE = 11.090-0.296 x %FAT-0.037 x pack-year). It was concluded that body fatness and smoking history substantially influence the thermic effect of smoking. In addition, this finding helps explain the wide range in TES which has been reported among subjects in many previous studies.

Potentiating effects of cigarette smoking and moderate exercise on the thermic effect of a meal.

The purposes of this study were: (i) to determine the relative thermic effects of smoking and exercise in fasted and postprandial states, and (ii) to determine whether there is a weight-controlling caloric advantage of moderate exercise in the postprandial state which might be used upon smoking cessation. The subjects were ten physically fit, young, male smokers. Twenty minutes of smoking (two cigarettes) while fasted resulted in a 6.0% (12.5 kcals/3h) increase in resting metabolic rate (RMR), and 20 minutes of walking (5.8 km/h) while fasted increased post-exercise RMR by 5.8% (11.7 kcals/3h). The thermic effect of a meal (TEM) (740 ml, 874 kcals) increased RMR 21.0% (42.3 kcals/3h), which was increased to 22.1% by smoking (45.0 kcals/3h). Exercise after a meal increased RMR 29.1% (58.1 kcals/3h). Post-prandial exercise potentiated the TEM, as the energy cost was 4.0 kcals/3h greater than the sum of the thermic effect of the meal plus the thermic effect of exercise in the fasted state. Postprandial exercise expended 112.2 kcals/20 min vs. 101.6 kcals/20 min for fasted exercise, a difference of 10.4%. The difference increased to 14.6% when the post-exercise thermic effect was included. It was concluded that the thermic effect of smoking and exercise were similar in the fasted state, but were substantially different postprandially. Moderate postprandial exercise appears to offer a substantial weight-controlling advantage when compared with fasted exercise.

Cigarette smoking and federal black lung benefits in bituminous coal miners.

The records of 1000 consecutive coal miners applying for benefits under the Federal Coal Mine Health and Safety Act were examined to determine the contribution of age, dust accumulation, and cigarette smoking to the profile of the miner who satisfies the current pulmonary criteria for disability. Using the presence of pneumoconiosis on chest radiograph as the indication of significant coal dust accumulation, the miners were separated into Group A--those without pneumoconiosis (n = 316) and Group B--those with pneumoconiosis (n = 684). The federal spirometric criteria for disability identified 55/316 miners in Group A (14.5%) and 99/684 miners in Group B (17.4%) potentially eligible for an award (P = .27). The mean ages of miners in both groups did not differ significantly, nor was there difference in the mean ages of groups that did or did not meet the federal criteria. In both groups, those miners potentially eligible for a financial award smoked more cigarettes than did their counterparts (Group A, 31.0 v 18.5 pack-years, P less than .001; Group B, 31.3 v 23.6 pack-years, P less than .001). There was no difference in the smoking histories of the miners from either group who met the federal criteria. Our data indicate that, in the case of bituminous coal miners, the present federal legislation intended to identify and remunerate those who suffer lung impairment from chronic occupational exposure to coal dust is biased in favor of those who sustain additional damage to their ventilatory capacity by smoking cigarettes.