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Coffee contains polyphenolic antioxidants and caffeine, which may favorably affect pulmonary function. Therefore, the authors studied cross-sectional associations (1987–1989) between coffee intake and pulmonary function in the Atherosclerosis Risk in Communities Study, a population-based cohort study (analytic sample=10,658). They also conducted analyses stratified by smoking status, since smoking is a strong risk factor for respiratory disease and could influence the effects of caffeine and antioxidants. Self-reported coffee intake was categorized as rare/never, <7 cups/week, 1 cup/day, 2–3 cups/day, and ≥4 cups/day. Pulmonary function was characterized by the spirometric measures forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1). After adjustment for demographic factors, lifestyle characteristics, and dietary factors, pulmonary function values increased across increasing categories of coffee consumption in never and former smokers but not in current smokers. In never or former smokers who consumed ≥4 cups of coffee daily, FVC and FEV1 were 2%–3% greater than in never or former smokers who rarely/never consumed coffee (Ptrend values: in never smokers, 0.04 for FVC and 0.07 for FEV1; in former smokers, <0.001 for FVC and <0.001 for FEV1). These data show a possible beneficial effect of coffee (or a coffee ingredient) on pulmonary function, but it appears to be limited to nonsmokers.
Chronic obstructive pulmonary disease (COPD) is characterized by a narrowing of the lung airways and consequent poor pulmonary function. The disease affects 12.1 million adults over the age of 25 years, and in 2007 it resulted in $42.6 billion in health-care costs and lost productivity (1). Compared with other chronic diseases with similar burdens on quality of life and health-care resources, less is known about how lifestyle factors (other than smoking (2)), such as diet, influence pulmonary function and the development of COPD. Although studies have been few, investigators who have analyzed the relation between diet and pulmonary function have reported statistically significant inverse associations between pulmonary function and intake of cured meats (3–5) and positive associations between pulmonary function and intake of polyunsaturated fatty acids (6), dietary fiber (especially from grain and vegetable sources) (7), fruit (8–10), vegetables (9), whole grains (8), and fish (10, 11).
There are limited data on the association between coffee consumption and pulmonary function. Coffee contains constituents that may have favorable effects on pulmonary function, such as caffeine, magnesium, and, most notably, several polyphenolic antioxidants (12). Despite widespread use of coffee and the potential beneficial effects, the association between pulmonary function and intake of coffee or caffeine has not been studied in the general population. To date, data on this topic have been derived mainly from experimental studies of small size and limited generalizability (13–15).
Smoking behavior may wield a strong influence on an association between coffee consumption and pulmonary function. First, smokers are often more frequent coffee drinkers (16), and smokers are also inherently at greater risk for pulmonary disease. Thus, coffee consumption could artificially appear to decrease pulmonary function. Smoking may also intercede in the pathways through which coffee constituents are hypothesized to mediate effects on pulmonary function. For example, smoking induces the enzyme cytochrome P-450 1A2, resulting in more rapid metabolism of caffeine (17–19). If caffeine and coffee-derived antioxidants are important mediators of the association between coffee consumption and pulmonary function or disease, it is possible that smoking overwhelms the effects of coffee intake on pulmonary function.
To investigate the associations among coffee consumption, smoking, and pulmonary function, we used data from the baseline examination of the Atherosclerosis Risk in Communities (ARIC) Study, a large, population-based cohort study. We hypothesized that coffee intake would be positively associated with pulmonary function and that associations would be stronger in nonsmokers.
The ARIC Study was initiated in 1987 and included African-American and white men and women aged 45–64 years who were recruited from 4 US communities: Forsyth County, North Carolina; Jackson, Mississippi; the northwestern suburbs of Minneapolis, Minnesota; and Washington County, Maryland (20). Participants (n=15,792; 8,710 women and 7,082 men) gave informed consent, and all protocols were approved by the institutional review board at each field center. In the cross-sectional investigation described here, we utilized pulmonary function measures (forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1)) and self-reported dietary intake data from the baseline examination (1987–1989). Participants were excluded from these analyses if they: 1) were not African-American or white (because of small numbers; n=48); 2) were missing data on pulmonary function or had a score of 0 (n=145); 3) did not have a pulmonary function test that passed quality control standards (n=2,543); 4) had self-reported physician-diagnosed asthma (n=926); 5) had self-reported physician-diagnosed chronic bronchitis or emphysema with an FEV1 (percent of predicted) less than 70 and an FEV1:FVC ratio less than 80 (to eliminate concomitant disease; n=327); 6) had values below the fifth percentile for any 1 of the following measures: percent of predicted FEV1, percent of predicted FVC, or FEV1:FVC ratio (to focus on a “healthy” sample; n=1,401); 7) provided insufficient dietary data (>10 missing items on the food frequency questionnaire (FFQ)) or had extreme energy intakes (<600 kcal or >4,200 kcal for men and <500 kcal or >3,600 kcal for women; approximate lower and upper 1 percentiles of the energy-intake distribution) (n=364); or 8) were missing data on coffee intake (n=18). After these exclusions (some of which overlapped), 10,658 participants remained for analysis (8,413 whites and 2,245 African Americans; 4,798 men and 5,860 women).
At the baseline examination, participants completed an interviewer-administered, 66-item semiquantitative FFQ, modified (21) from the 61-item FFQ designed and validated by Willett et al. (22). Using an 8-ounce (0.24-L) cup as a visual reference for intake estimation, participants were asked how frequently they consumed regular (not decaffeinated) coffee. Frequency options were the following: almost never, 1–3 cups per month, 1 cup per week, 2–4 cups per week, 5–6 cups per week, 1 cup per day, 2–3 cups per day, 4–5 cups per day, and ≥6 cups per day. To estimate associations with pulmonary function variables, we combined some of these frequency options to create a 5-level categorical coffee intake variable (almost never, <1 cup per day, 1 cup per day, 2–3 cups per day, and ≥4 cups per day), consistent with previous ARIC analyses (23).
Demographic characteristics, behavioral/lifestyle factors, and clinical data were obtained from each subject at baseline. Ethnicity was self-reported. Detailed information on cigarette smoking and history of respiratory disease was obtained through interview-administered questionnaires. For this analysis, never smokers were defined as participants who had not smoked more than 400 cigarettes in their lifetime. Former smokers were participants who had quit smoking at least 1 year prior to the interview. Self-reported respiratory symptoms were ascertained with a standardized questionnaire adapted from the Epidemiology Standardization Project (24). Respiratory disease was also self-reported, but a participant responding in the affirmative was asked whether his/her disease had been diagnosed/confirmed by a physician. Pulmonary function testing was completed under fasting conditions (no food or drink, including coffee; only water was allowed).
Pulmonary function was measured by trained and certified technicians according to American Thoracic Society criteria, using a standardized protocol (24, 25), and all results were interpreted at a single reading center. Participants performed the FVC maneuver until there were 2 error-free reproducible maneuvers (FEV1 and FVC within 5%) out of 3 acceptable maneuvers, with the maneuvers being repeated up to 8 times if necessary. Percent of predicted FEV1 and FVC were computed using sex- and race-specific prediction equations that included height and age (26).
Poor pulmonary function was defined by an FEV1:FVC ratio less than 0.7 and an FEV1 less than 80% of that predicted on the basis of spirometry tests (postbronchodilator values were not available).
Analysis of variance was used to evaluate participant characteristics according to categories of reported coffee intake. Differences among categories were determined by F tests (continuous variables) or chi-squared tests (categorical variables). Linear regression was used to characterize the relations between coffee intake and the pulmonary function variables FEV1 and FVC, quantified both in liters and as percent of predicted. P for trend across categories was determined by modeling the categorical coffee variable continuously (ordinal variable with values 0–4). Logistic regression was used to estimate odds ratios and 95% confidence intervals for COPD across coffee intake categories, with rare/never consumers being used as the referent group.
Two multivariable models were used for these analyses. In model 1, results were adjusted for field center, sex, age, race, physical activity level (in leisure time and in sports activities (27)), smoking status (current, former, or never smoker), cigarette years (average number of cigarettes smoked per day × number of years of smoking), and body mass index (weight (kg)/height (m)2). Model 2 included the variables in model 1, plus energy intake (kcal/day) and intakes of nutrients shown previously in ARIC to be associated with pulmonary function: n-3 polyunsaturated fatty acids (g/day) (6) and dietary fiber (g/day) (7). Data were unchanged after additional adjustment for other dietary factors, such as intakes of processed meat, fish, fruits and vegetables, and whole grains; therefore, those results are not presented.
We also stratified these analyses by smoking status, using the models outlined above (minus smoking status). We conducted a formal test of interaction between smoking status and coffee intake by including a smoking status × coffee intake interaction term in the fully adjusted model (model 2).
Mean coffee consumption was approximately 2 cups per day, with 26% of participants reporting rarely or never consuming coffee and 17% reporting consuming 4 or more cups each day (extreme categories of intake). In general, frequent coffee drinkers were more likely to be current smokers, younger, male, and white, to have a lower body mass index, and to be more physically active than less frequent coffee drinkers (P<0.05 for all; Table 1). Dietary differences across categories of coffee intake were also evident, with less healthful dietary habits (i.e., lower intake of whole grains, fruits and vegetables, and fish but higher intake of processed meat) being characteristic of persons more frequently consuming coffee (P<0.05 for all).
Pulmonary function values were statistically significantly higher across increasing categories of coffee intake in all participants (P for trend < 0.001; Table 2). After adjustment for demographic and lifestyle factors (model 1), participants consuming at least 4 cups of coffee per day had an approximately 2% higher FEV1 and approximately 3% higher FVC values than participants who never or only rarely consumed coffee (difference of approximately 0.06–0.09 L). Results were similar for percent of predicted FEV1 and FVC, with higher values being observed in regular coffee drinkers than in infrequent coffee drinkers. However, the association between coffee intake and the FEV1:FVC ratio was reversed (P for trend=0.04). These results were similar when further adjusted for energy intake and other nutrients (model 2) or food covariates (data not shown), except that the association between coffee intake and the FEV1:FVC ratio was no longer significant (P for trend=0.07).
When data were stratified by smoking status, trends across coffee intake categories were statistically significant among never or former smokers but not current smokers (Table 3). The trend for the ratio of FEV1 to FVC across categories of coffee intake was not statistically significant for any of the specific smoking strata (Table 3). Although P values from many of the trend tests were statistically significant, the P value from the formal test for interaction between coffee intake and smoking status was not statistically significant (P for interaction ≥ 0.42; see Table 3). When former smokers were stratified by duration of cessation (number of years since quitting smoking), the association between coffee intake and pulmonary function was weaker in persons who had quit smoking within the previous 15 years as compared with those who had quit smoking 15 or more years previously (Table 4). However, again, there was not a statistically significant interaction between coffee intake and the duration of smoking cessation (P for interaction ≥ 0.21; see Table 4).
After exclusion of self-reported physician-diagnosed respiratory disease, the overall prevalence of spirometry-defined COPD was fairly low (4.6%), but, as expected, COPD was more common in current smokers (11.3%) than in never smokers (1.49%). Although coffee consumption was positively associated with continuous measures of pulmonary function, there were no statistically significant associations between coffee intake and spirometry-defined COPD (Table 5).
In this large, population-based cohort, coffee consumption was positively associated with pulmonary function. This association was observed in only never smokers and long-term quitters, minimizing the possibility of confounding by smoking, which is known to affect pulmonary function (2) and be correlated with coffee consumption (16).
The interaction between smoking status and coffee consumption was not statistically significant. However, associations between coffee consumption and pulmonary function were statistically significant in never smokers and former smokers but not significant in current smokers. There are several possible biologic mechanisms that may explain our findings. First, the influence of coffee consumption on pulmonary function may be overwhelmed by the known deleterious effects of smoking on pulmonary function and thus may only be detectable in persons who have never smoked or whose duration of smoking cessation is relatively long. Second, our findings may suggest that caffeine is the constituent in coffee that is responsible for the observed associations with pulmonary function and that smoking counters the potential effect of caffeine by accelerating its metabolism and clearance (28–30). The hypothesis that caffeine favorably affects pulmonary function is supported by previous studies showing improved pulmonary function following caffeine supplementation in persons with pulmonary diseases (13, 15). Caffeine is structurally similar to the therapeutic agent theophylline, which is used to treat obstructive airway diseases and may have beneficial effects on pulmonary function by increasing respiratory muscle strength and prolonging time to diaphragmatic fatigue (13, 14)—although the levels of such compounds tested in studies investigating these effects are much greater than the levels in coffee beverages, possibly implying that coffee constituents in addition to, or other than, caffeine are involved. Third, our findings may suggest that the absence of association between coffee intake and pulmonary function in smokers is due to a dampened effect of coffee-derived antioxidants on pulmonary function in smokers who have a lower baseline plasma antioxidant level (even when controlling for differences in dietary antioxidant intake) due to a greater oxidative burden incurred by smoking (31). Previous studies have shown that inflammation is involved in the pathophysiology of reduced pulmonary function (32) and that associations between dietary intake and pulmonary function are thought to be mediated, in part, by antiinflammatory/antioxidative mechanisms (6–8, 33–36). Several polyphenolic compounds in coffee and their metabolites have antiinflammatory and antioxidative properties (12, 37, 38). Thus, the associations between coffee intake and pulmonary function (in nonsmokers) may be related to coffee beverages as a whole or a particular coffee constituent with antioxidative/antiinflammatory properties—an effect that may be overwhelmed in the inflammatory milieu created by smoking.
Limitations of our investigation deserve discussion. Ours was a cross-sectional analysis with dietary intake and lung function measured only at the baseline examination. Therefore, we cannot define the time course of these associations, although we did attempt to minimize the potential for reverse causal associations to bias our findings; for example, we excluded persons with very low measured pulmonary function whose dietary intakes may have been consequently modified. With 95% power and a 2-sided significance level of 5%, this analysis had statistical power to detect an odds ratio of 1.78 for persons in the highest quartile of coffee intake. However, we did not observe an association between coffee consumption and spirometry-defined COPD. This may be due to our use of a fairly healthy sample with few spirometry-defined COPD cases or simply to the fact that the impact of smoking far outweighs that of coffee drinking when overt clinical COPD, which was rare in never smokers (<2% of our sample), is considered as the outcome. Although the differences in measures of lung function across categories of coffee intake were small, differences of this magnitude have been associated with cardiovascular disease risk factors in this cohort (39). Thus, the pathology underlying these small differences may have important implications for overall health. Lastly, despite adjustment for smoking status and cigarette years of smoking, residual confounding by incomplete characterization of smoking behavior is possible; thus, we emphasize the statistically significant associations observed in never smokers.
We also note that the FFQ used in the ARIC Study was less comprehensive than FFQs used in other studies (3, 5, 8, 9). While this should not have affected our assessment of coffee intake, it could have influenced the accuracy of data on other confounding dietary factors. However, such measurement error probably does not fully explain our findings, since associations were not affected by adjustment for other nutrients or foods shown in the ARIC cohort or other cohorts to be associated with pulmonary function. Furthermore, the accuracy of participants’ reported habitual intake of beverages (e.g., coffee (40)) is likely to be greater than that for foods consumed intermittently (41). Our confidence in the accuracy of coffee assessment in the ARIC cohort is also bolstered by another ARIC investigation demonstrating coffee-disease associations (23), which is consistent with other studies utilizing alternative FFQ formats (40). While we cannot exclude the possibility of misclassification of coffee intake, we do not suspect systematic reporting bias in accordance with lung function measurements. Thus, any misclassification would probably have been random, resulting in attenuated risk estimates. Lastly, we were unable to investigate the independent contribution of coffee constituents other than caffeine, since decaffeinated coffee intake was not quantified by the FFQ used in ARIC.
In this cross-sectional analysis, coffee consumption was positively associated with measures of pulmonary function in persons who had never smoked or who were long-term quitters but not among current smokers. These data suggest that smoking may intercede in pathways related to pulmonary function that are putatively affected by coffee constituents, such as caffeine and polyphenolic antioxidants. Alternatively, smoking may obscure any beneficial effect of coffee consumption on pulmonary function simply on the basis of its strength as a risk factor.
Authors' affiliation: Division of Epidemiology and Disease Control, University of Texas Health Science Center, Houston, Texas (Jennifer A. Nettleton, Jack L. Follis, Matthew B. Schabath).
The Atherosclerosis Risk in Communities (ARIC) Study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, and N01-HC-55022.
The authors thank the staff of the ARIC Study for their important contributions.
Conflict of interest: none declared.