Cigarette smoking is associated with a greater risk of incident asthma in allergic rhinitis.

BACKGROUND: Asthma and rhinitis are often comorbid conditions, and several studies have suggested that rhinitis often precedes asthma. Sensitization to allergen has been shown to be one of the strongest determinants of incident asthma, but little is known about the effects of cigarette smoking among individuals with allergic rhinitis. OBJECTIVE: We sought to evaluate the importance of cigarette smoking as an additional risk factor for incident asthma in a cohort of hospital-referred nonasthmatic adult subjects with allergic rhinitis. METHODS: The study population selected at baseline was invited for a follow-up visit 10 years later to check for possible asthma features. Categories of smokers, exsmokers, and never smokers were used in the analyses together with pack-years to calculate the level of cumulative exposure. RESULTS: Complete data were available from 325 patients. Smoking was significantly related to the risk of incident asthma, with the odds ratio (OR) being 2.67 (95% CI, 1.70-4.19) for univariate and 2.98 (95% CI, 1.81-4.92) for multivariate analyses. A clear dose-response association for exposure to tobacco and risk of new-onset asthma was observed in the multivariate analyses: those with 1 to 10 pack-years had an OR of 2.05 (95% CI, 0.99-4.27), those with 11 to 20 pack years had an OR of 3.71 (95% CI, 1.77-7.78), and those with 21 or more pack-years had an OR of 5.05 (95% CI, 1.93-13.20) compared with never smokers. CONCLUSIONS: The current findings support the hypothesis that cigarette smoking is an important independent risk factor for the development of new asthma cases in adults with allergic rhinitis.

The change in excess risk of lung cancer attributable to smoking following smoking cessation: an examination of different analytic approaches using CPS-I data.

BACKGROUND: Lung cancer risk is modified by smoking cessation. However, the inclusion in the group of former smokers of those who quit after developing symptoms or being diagnosed with lung cancer distorts the apparent risk in the first several years following cessation. This bias is termed the quitting ill effect. METHODS: Lung cancer mortality data from the American Cancer Society's CPS-I were used to calculate the excess mortality among white male former smokers compared to the predicted risk had those individuals continued to smoke. Alternate approaches to minimizing the quitting ill bias were investigated. Goodness-of-fit of the models was assessed graphically and formally. RESULTS: Poisson models were built for the absolute lung cancer risk for never smokers and the excess risk, over never smokers, for continuing smokers. The decrease in excess risk in former smokers was modeled by a negative exponential function. The models for the three smoker subgroups (continuing, never, and former), all fit the data well. Assuming that the fraction of excess risk remaining for former smokers does not decline for the first two years following cessation and that the quitting ill effect does not influence those who are five or more years post-cessation allowed a reasonable estimation of the change in risk of lung cancer with increasing duration of abstinence. CONCLUSIONS: The reduction in the excess risk of lung cancer in former smokers can be estimated, and the quitting ill effect minimized, by the inclusion of a lag between cessation and onset of reduction in risk.

Risk factors for progression of peripheral arterial disease in large and small vessels.

BACKGROUND: Data on the natural history of peripheral arterial disease (PAD) are scarce and are focused primarily on clinical symptoms. Using noninvasive tests, we assessed the role of traditional and novel risk factors on PAD progression. We hypothesized that the risk factors for large-vessel PAD (LV-PAD) progression might differ from small-vessel PAD (SV-PAD). METHODS AND RESULTS: Between 1990 and 1994, patients seen during the prior 10 years in our vascular laboratories were invited for a new vascular examination. The first assessment provided baseline data, with follow-up data obtained at this study. The highest decile of decline was considered major progression, which was a -0.30 ankle brachial index decrease for LV-PAD and a -0.27 toe brachial index decrease for SV-PAD progression. In addition to traditional risk factors, the roles of high-sensitivity C-reactive protein, serum amyloid-A, lipoprotein(a), and homocysteine were assessed. Over the average follow-up interval of 4.6+/-2.5 years, the 403 patients showed a significant ankle brachial index and toe brachial index deterioration. In multivariable analysis, current smoking, ratio of total to HDL cholesterol, lipoprotein(a), and high-sensitivity C-reactive protein were related to LV-PAD progression, whereas only diabetes was associated with SV-PAD progression. CONCLUSIONS: Risk factors contribute differentially to the progression of LV-PAD and SV-PAD. Cigarette smoking, lipids, and inflammation contribute to LV-PAD progression, whereas diabetes was the only significant predictor of SV-PAD progression.

Does a failed quit attempt reduce cigarette consumption following resumption of smoking? The effects of time and quit attempts on the longitudinal analysis of self-reported cigarette smoking intensity.

California Tobacco Survey respondents were asked the intensity of their cigarette smoking 1 year previously and at the time of the survey. Respondents reported a generally lower smoking intensity at survey time compared with 1 year previously. Multivariable statistical models on the change in smoking intensity in the past year were fitted to assess the effects of low-tar cigarette use, a quit attempt in the past year, smoking intensity 1 year previously, and demographic variables (age, education, income, and race). The most important predictor of change in intensity was the intensity 1 year previously. The next most important predictor was whether a quit attempt had been made in the previous year. The demographic variables also were found to have a significant effect, although their effects were of smaller magnitude. Low-tar cigarette use was not a significant predictor of change in intensity in multivariable analysis. The effect of a quit attempt on the reduction in intensity of smoking suggests that periods of cessation may reduce the intensity of smoking and the level of addiction for several months following relapse. Consequently, it may be important to control for cessation activity in studies comparing exposures from conventional tobacco products to exposures from new products that purport to offer lower harm.

Lung cancer mortality is related to age in addition to duration and intensity of cigarette smoking: an analysis of CPS-I data.

OBJECTIVES: Models previously developed for predicting lung cancer mortality from cigarette smoking intensity and duration based on aggregated prospective mortality data have employed a study of British doctors and have assumed a uniform age of initiation of smoking. We reexamined these models using the American Cancer Society's Cancer Prevention Study I data that include a range of ages of initiation to assess the importance of an additional term for age. METHODS: Model parameters were estimated by maximum likelihood, and model fit was assessed by residual analysis, likelihood ratio tests, and chi(2) goodness-of-fit tests. RESULTS: Examination of the residuals of a model proposed by Doll and Peto with the Cancer Prevention Study I data suggested that a better fitting model might be obtained by including an additional term specifying the ages when smoking exposure occurred. An extended model with terms for cigarettes smoked per day, duration of smoking, and attained age was found to fit statistically significantly better than the Doll and Peto model (P < 0.001) and to fit well in an absolute sense (goodness-of-fit; P = 0.34). Finally, a model proposed by Moolgavkar was examined and found not to fit as well as the extended model, although it included similar terms (goodness-of-fit; P = 0.007). CONCLUSIONS: The addition of age, or another measure of the timing of the exposure to smoking, improves the prediction of lung cancer mortality with Doll and Peto's multiplicative power model.

Weight loss: a determinant of hip bone loss in older men and women. The Rancho Bernardo Study.

The sex-specific effect of weight change on change in total hip bone mineral density was evaluated over 4 years (1992-1996) in 1,214 community-dwelling adults whose mean age at baseline was 71 years. Weight and bone mineral density (by dual-energy x-ray absorptiometry) were assessed at two study visits. The average bone loss was 0.5% per year in both sexes; 29% of men and 28% of women lost at least 1% of bone mineral density per year. More than one in five participants lost at least 1% of their body weight per year (21% of men and 23% of women). These weight losers were twice as likely as others to lose bone at the rate of at least 1% per year. In analyses controlling for age, baseline weight, and lifestyle, weight loss was the strongest independent predictor of bone loss (odds ratios were 1.53 for men and 1.56 for women). Persons with weight loss of at least 1% per year were more likely to report fair or poor health and functional limitation at the second visit and to die within 2 years of the second visit; however, most did not report declining health, and most survived for at least 2 additional years.

The relationship between weight loss and all-cause mortality in older men and women with and without diabetes mellitus: the Rancho Bernardo study.

OBJECTIVES: To examine the relationship between measured weight change over an approximate 10-year time period on all-cause mortality over the following 12 years in 1,801 community-dwelling men and women (mean age 71 at the beginning of mortality follow-up) with and without diabetes mellitus. DESIGN: A longitudinal cohort study. SETTING: A geographically defined community in southern California. PARTICIPANTS: One thousand eight hundred one older men and women with and without diabetes mellitus. MEASUREMENTS: Weight, body mass index (BMI), blood pressure, and fasting plasma glucose were measured in 1972-74 (Visit 1) when participants were aged 40 to 79 and again in 1984-87 (Visit 2). Lifetime weight history and dieting for weight control were ascertained in 1985 using a mailed questionnaire. Vital status was determined for the next 12 years, from Visit 2 (1984-87) through 1996. The Cox proportional hazards model was used to assess the age- and multiply adjusted effect of weight change on mortality. RESULTS: At Visit 1, diabetic men (n = 140) and women (n = 90) were more overweight than nondiabetic men (n = 633) and women (n = 938). Weight gain between Visits 1 and 2 was not a significant predictor of mortality in this cohort. Men and women losing 10 or more pounds between visits had higher age-adjusted death rates during the following 12 years than those with stable weight or weight gain. Weight loss was associated with an increased hazard ratio (HR) for all-cause mortality in nondiabetic men (HR = 1.38, 95% confidence interval (CI) = 1.06-1.80) and women (HR = 1.76, 95% CI = 1.33-2.34) and diabetic men (HR = 3.66, 95% CI = 2.15-6.24) and women (HR = 1.65, 95% CI = 0.70-3.87) after adjustment for age, smoking, and sedentary lifestyle. Significant associations persisted in analyses excluding cigarette smokers and those with depressed mood and low baseline BMI. After excluding those who died within 5 years of the weight loss, the increased HR was statistically significant in men and women with and without diabetes mellitus. Stratified analyses comparing those who reported dieting for weight control with those not dieting showed similar trends, with a higher mortality risk for weight loss in those who lost weight without dieting. CONCLUSION: In this population of older individuals, weight loss predicted increased all-cause mortality risk not explained by covariates.

Stability of electrocardiographic classification pre- and postglucose challenge.

Because of validity concerns, electrocardiograms (ECGs) in epidemiologic studies are usually taken in fasting subjects. It would be preferable logistically to record ECGs throughout the day. The authors investigated the stability of ECGs taken while fasting and approximately 1 hour after a 75-g glucose load on the same morning in 89 older men and women who were participants in the Rancho Bernardo (California) Chronic Disease Study between 1984 and 1995. A reader blinded to this comparison classified ECGs using the Minnesota code and Whitehall criteria. Of 75 initially normal tracings, 27% changed to possible ischemia postglucose. Of 12 tracings initially indicating possible ischemia, two reverted to normal (kappa = 0.40, 95% confidence interval: 0.21, 0.59). The two tracings initially scored as probable ischemia remained in that category postglucose. More ECGs worsened than improved, and the variability pre- and postglucose was at least as great as that between clinic visits conducted 8 years apart.