Combined Effects Of Smoking Research Articles

Longitudinal decline in lung function in former asbestos exposed workers

BackgroundThis study was designed to assess the effect of asbestos exposure on longitudinal lung function decline.MethodsA group of 502 former asbestos-cement workers with at least two spirometry tests 4 years...

Localized pleural thickening: Smoking and exposure to Libby vermiculite

There is limited research on the combined effects of smoking and asbestos exposure on risk of localized pleural thickening (LPT). This analysis uses data from the Marysville cohort of workers occupationally exposed to Libby amphibole asbestos (LAA). Workers were interviewed to obtain work and health history, including ever/never smoking and chest X-rays. Cumulative exposure estimates were developed on the basis of fiber measurements from the plant and work history. Benchmark concentration (BMC) methodology was used to evaluate the exposure-response relationship for exposure to LAA and a 10% increased risk of LPT, considering potential confounders and statistical model forms. There were 12 LPT cases among 118 workers in the selected study population. The mean exposure was 0.42 (SD=0.77) fibers/cc-year, and the prevalence of smoking history was 75.0% among cases and 51.9% among non-cases. When controlling for LAA exposure, smoking history was of borderline statistical significance (P-value=0.099), and its inclusion improved model fit, as measured by Akaike's Information Criterion. A comparison of BMC estimates was made to gauge the potential effect of smoking status. The BMC was 0.36 fibers/cc-year, overall. The BMC for non-smokers was approximately three times as high (1.02 fibers/cc-year) as that for the full cohort, whereas the BMC for smokers was about 1/2 that of the full cohort (0.17 fibers/cc-year).

Interaction of smoking and metabolic syndrome on cardiovascular risk in a Chinese cohort

BackgroundThe high prevalence of smoking and metabolic syndrome (MS) and increased incidence of cardiovascular disease (CVD) in China indicates that there may be an interaction between smoking and MS on cardiovascular risk. Therefore, we aimed to examine the independent and combined effects of smoking and MS on risk of CVD in a Chinese cohort. MethodsWe analyzed data from a population-based prospective cohort of 3598 participants aged 35–74years from Jiangsu China who were free of diabetes and CVD at enrollment and were followed for cardiovascular events (including myocardial infarction, ischemic stroke, hemorrhagic stroke, and cardiovascular mortality) until 31 August 2008. ResultsDuring 8years (median 6.3years) of follow-up, 82 participants developed CVD. After adjusting for age, sex, body mass index, alcohol consumption, family history of cardiovascular disease and MS, smoking significantly increased cardiovascular risk in a dose–response manner. After further adjustment for smoking status, the hazard ratio of CVD for participants with MS was 2.49 (95% confidence interval 1.59–3.90) compared with those without the syndrome. There was a statistically significant additive interaction between current smoking and MS on cardiovascular risk. The risk of CVD for current smokers with MS was 1.81 times as high as the sum of risks in participants with a single condition alone. ConclusionsBoth cigarette smoking and MS are strong risk factors of CVD in the Chinese population. Moreover, this study further demonstrates an additive interaction of current smoking and MS on cardiovascular risk.

Abstract B31: Gene-based lung cancer risk test (Respiragene), identifies high-risk smokers for early detection of lung cancer

Abstract Lung cancer results from the combined effects of smoking and genetic susceptibility. Recent studies show that between 50-90% of lung cancer cases have preexisting COPD and reduced FEV1 has been shown to be the single most important risk factor for lung cancer among smokers. Given the heritability for COPD and lung cancer is 40-75% and 15-25% respectively, it is clear genes conferring risk of COPD also underlies lung cancer susceptibility. In a study of 930 subjects, we have developed a gene-based lung cancer susceptibility model that combines genetic markers (SNPs) associated with COPD and lung cancer, with non-genetic variables (age and family history), to derive a score that helps to distinguish those smokers (and ex-smokers) at greatest risk of lung cancer. The panel includes SNPs validated in candidate and GWAS studies. In a prospective study of 1212 smokers we identified 52 new lung cancers and show their lung cancer scores are very similar to that of the original lung cancer cases (n=446). In a 2nd cross-sectional study of 606 lung cancer cases from the United Kingdom, the lung cancer score was also similarly distributed and showed similar performance in an ROC analysis. In a CT study of 25 lung cancer detected through CT screening in Spain, a similar high score was shown. Current CT screening programs for lung cancer generally target smokers over 50 years with a minimum 20 pack year history and achieve pick up rates of 1%. Using our gene-based model, where age, family history, COPD and genetic variants are combined, lung cancer detection rates maybe even higher. Citation Information: Cancer Prev Res 2010;3(12 Suppl):B31.

Combined effects of smoking, anti-EBNA antibodies, and HLA-DRB1*1501 on multiple sclerosis risk

To examine the interplay between smoking, serum antibody titers to the Epstein-Barr virus nuclear antigens (anti-EBNA), and HLA-DR15 on multiple sclerosis (MS) risk. Individual and pooled analyses were conducted among 442 cases and 865 controls from 3 MS case-control studies-a nested case-control study in the Nurses' Health Study/Nurses' Health Study II, the Tasmanian MS Study, and a Swedish MS Study. Conditional logistic regression models were used to calculate odds ratios (ORs) and 95% CIs for the association between smoking, anti-EBNA titers, HLA-DR15, and MS risk. Study estimates were pooled using inverse variance weights to determine a combined effect and p value. Among MS cases, anti-EBNA titers were significantly higher in ever smokers compared to never smokers. The increased risk of MS associated with high anti-EBNA Ab titers was stronger among ever smokers (OR = 3.9, 95% CI = 2.7-5.7) compared to never smokers (OR = 1.8, 95% CI = 1.4-2.3; p for interaction = 0.001). The increased risk of MS associated with a history of smoking was no longer evident after adjustment for anti-EBNA Ab titers. No modification or confounding by HLA-DR15 was observed. The increased risk of MS associated with ever smoking was only observed among those who had high anti-EBNA titers (OR = 1.7, 95% CI = 1.1-2.6). Smoking appears to enhance the association between high anti-EBNA titer and increased multiple sclerosis (MS) risk. The association between HLA-DR15 and MS risk is independent of smoking. Further work is necessary to elucidate possible biologic mechanisms to explain this finding.

Combined Effects of Smoking and Systolic Blood Pressure on Risk of Coronary Heart Disease: A Cohort Study in Chinese Women

To quantify the combined effects of systolic blood pressure (SBP) and cigarette smoking on incident coronary heart disease (CHD) in women. Overall, 86,338 women aged >or=40 years were enrolled in 1991. The follow-up evaluation was conducted in 1999-2000, with a response rate of 92.9%. A total of 829 CHD events (fatal and nonfatal) were observed among the participants who were free of cardiovascular diseases (CVD) at baseline. Higher SBP was significantly associated with more risk of CHD in both nonsmokers and current smokers (all p < 0.0001 for linear trends). Comparing with never smoking, both low and high levels of cigarettes smoked per day (1-7, and >or=8 cigarettes per day) and pack-years (<10, and >or=10 pack-years) were associated with increased risk of CHD in those with normal and high SBP. The multivariate adjusted relative risks (RRs) of CHD were 2.54 (95% confidence interval [CI] 2.00-3.23), 1.28 (1.01-1.63), and 1.57 (1.33-1.86) for current smokers with high SBP, current smokers with normal SBP, and nonsmokers with high SBP, respectively, compared with nonsmokers with normal SBP. The present study identified a statistically significant additive interaction between these two factors on CHD. Our study indicated that the combined effects of cigarette smoking and high SBP could be expected to have extra adverse effects on CHD in women, which highlights the importance of multifactorial interventions to decrease the risk of CHD, for example, quitting smoking and treatment of high blood pressure in Chinese women.

Combined effects of smoking, coffee, and NSAIDs on Parkinson's disease risk

Inverse associations of Parkinson's disease (PD) with cigarette smoking, coffee drinking, and nonsteroidal anti-inflammatory drug (NSAID) use have been reported individually, but their joint effects have not been examined. To quantify associations with PD for the individual, two-way and three-way combinations of these factors, a case-control association study with 1,186 PD patients and 928 controls was conducted. The study setting was the NeuroGenetics Research Consortium. Subjects completed a structured questionnaire regarding smoking, coffee, and NSAID consumption. Odds ratios were calculated using unconditional logistic regression. Smoking, coffee, and over the counter NSAID use as individual factors exhibited significantly reduced risks of 20% to 30%. The two-way and three-way combinations were associated with risk reduction of 37% to 49%, and 62%, respectively. Smoking and coffee exhibited significant inverse risk trends with increasing cumulative exposures, suggesting dose-response relations. With respect to the combination of all three exposures, persons who were at the highest exposure strata for smoking and coffee and used NSAIDs had an estimated 87% reduction in risk (OR = 0.13, 95% CI = 0.06-0.29). Whether this finding reflects true biologic protection needs to be investigated.

The effect of smoking and hypertensive disorders on abruptio placentae in Norway 1999–2002

To assess the effects of smoking and hypertension on abruptio placentae and whether the effect of hypertension is modified by smoking and vice versa. To quantify the proportion of abruptio placentae cases attributable to hypertension and smoking. Registry based national cohort study. 814 cases of abruptio placentae among a total of 211,868 births in Norway during the period 1999-2002. Logistic regression analysis was used to assess whether the risk of abruptio placentae is influenced by maternal smoking habits and hypertensive disorders and to evaluate interactions in the effects on abruptio placentae of smoking and hypertension. In occasionally and daily smokers at the onset of pregnancy, abruptio placentae occurred in 5.4 and 5.7 per 1000, respectively, against 3.4 per 1000 in non-smokers (adjusted odds ratios (ORs) for maternal age and birth order 1.6-1.7). No significant dose-response effect was found. Adjusted ORs for abruptio placentae in women with pre-eclampsia superimposed on chronic hypertension, transient hypertension, mild and severe pre-eclampsia, and pre-eclampsia with onset before 34th weeks of gestation were significantly increased (ORs 1.6-4.1). The combined effects of smoking and hypertensive disorder were additive. Hypertension explained 3.3% of abruptio placentae, while smoking explained 6.9% of abruptio placentae cases. The effects on abruptio placentae of hypertensive pregnancy disorders and smoking are independent and additive, indicating that smoking and hypertension have their effects though separate mechanisms. If smoking were eliminated in pregnant women, the number of abruptio placentae cases would be reduced by 7%.

The Effect of Health Compromising Behaviors on Preterm Births

The objective of our study was to determine whether there were combined effects of smoking, alcohol, and illicit drug use during pregnancy on the frequency of preterm births, and if so, the magnitude of the association after adjusting for confounding factors. We conducted a retrospective cohort study of singleton live births in Kansas City, Missouri from 1990-2002. We defined health compromising behaviors as the use of cigarettes, alcohol, and illicit drugs. The effect of these behaviors on preterm births was considered for each substance individually, and in combination. The rates of preterm births for these groups were calculated. Using logistic regression, adjusted odds ratios were used to estimate the relative risk of preterm births among these groups. Over 13% of infants born to women who smoked were preterm, compared to 9.6% for non-smokers. Of infants born to women who reported alcohol use, 17.3% were preterm compared to 10.1% for non-drinkers. Smoking and alcohol use in combination was associated with 18.0% preterm births, while alcohol and drug use in combination was associated with 20.8% preterm births. The use of all three substances was associated with 31.4% preterm births. Women who engaged in health compromising behaviors during pregnancy showed an increased proportion of preterm births compared to those who did not. There is significant interaction between these behaviors leading to higher rates of preterm births than predicted by their additive effects. To decrease preterm births, we must deal with the effects of smoking, drinking, and drug use simultaneously.

The effects of smoking and hypertensive disorders on fetal growth

BackgroundIt is well known that smoking and pregnancy induced hypertension (PIH) are associated with decreased fetal growth. It has been reported that in preeclampsia the fetal growth deficit attributable to smoking is higher, which has been contradicted in other studies. We therefore evaluated the effects on fetal growth of early- and late onset PIH and chronic hypertension and how cigarette smoking modify these effects. We also quantified the proportion of small for gestational age (SGA) cases attributable to PIH, chronic hypertension, and smoking.MethodsPopulation-based study based on record of 215598 singleton pregnancies from the Medical Birth Registry of Norway.ResultsIn severe preeclampsia, mild preeclampsia, transient hypertension, and normotension in term birth, odds ratios (ORs) of SGA in smokers compared with non-smokers were 1.4 (95% confidence interval 0.9, 2.2), 1.6 (1.3, 1.9), 2.3 (1.8, 3.1), and 2.0 (1.9, 2.1), respectively. For preterm births, corresponding ORs were 1.3 (0.9, 2.0), 1.8 (1.1, 3.0), 4.1 (1.9, 9.0), and 1.7 (1.4, 2.0), respectively. The effect of early onset PIH was stronger than that in term births, while the effect of smoking was equal in preterm and term newborns. Only in non-smokers who delivered at term, the rates of SGA significantly increased with the severity of PIH (ORs = 1.3 (1.1, 1.5), 1.8 (1.7, 2.0), and 2.5 (2.2, 3.0) for transient hypertension, mild-, and severe preeclampsia, respectively). The combined effects of smoking and hypertension were generally not synergistic. The effect of smoking was not stronger in women who had chronic hypertension. Nor were the effects of chronic hypertension stronger in smokers. PIH explained 21.9 and 2.5% of preterm and term cases of SGA, respectively, while smoking explained 12% of SGA cases.ConclusionThe effects of hypertensive disorder and smoking were generally not synergistic, which suggest that they may exert their main actions on separate sites or work through separate mechanisms within or outside the placenta. If smoking were eliminated in pregnant women, the number of SGA cases would be reduced by 12%.

The influence of erythrocyte folate and serum vitamin B12status on birth weight

The extent to which maternal folate and vitamin B12 modulate infant birth weight is unclear. The present study investigated mothers in early gestation (mean 11.5 (sd 5.8) weeks) and neonates, at delivery. Erythrocyte (RBC) folate (mothers: n 683; neonates: n 614) and vitamin B12 (mothers: n 534; neonates: n 614) were measured. Data on smoking habits were available for 44 % of pregnancies (n 443). The relationship between vitamin levels and birth weight standardized for gender and gestational age was investigated, using linear regression and adjusting for possible confounding variables (maternal age, parity). Results are presented as standardized regression coefficients (b). Increasing maternal age was associated with elevated RBC folate (b 0.11 (95 % CI 0.08, 0.15), P<0.001; n 674) and smoking was associated with a decrease in maternal RBC folate (b -1.38 (95 % CI -1.92, -0.86), P=0.001; n 319). Neonatal RBC folate was predicted by maternal RBC folate (b 0.08 (95 % CI 0.04, 0.11), P=0.001; n 315) and maternal vitamin B12 (b 0.08 (95 % CI 0.01, 0.16), P=0.02; n 252). Smoking influenced maternal vitamin B12 status (b -0.88 (95 % CI -1.49, -0.27), P=0.005; n 231). Using univariate regression, smoking significantly influenced infant birth weight (b -2.15 (95 % CI -3.24, -1.04), P<0.001; n 437). However, the effect of smoking on birth weight was statistically non-significant when considered in a multivariate regression model, leaving maternal RBC folate as the only significant predictor of birth weight (b 0.25 (95 % CI 0.08, 0.42), P=0.005; n 145). These findings suggest that maternal folate status is an important determinant of infant birth weight. The combined effects of smoking and reduced RBC status on birth weight require further investigation.

Effects of subfertility cause, smoking and body weight on the success rate of IVF

We investigated the separate and combined effects of smoking and body mass index (BMI) on the success rate of IVF for couples with different causes of subfertility. The success rate of IVF was examined in 8457 women. Detailed information on reproduction and lifestyle factors was combined with medical record data on IVF treatment. All IVF clinics in The Netherlands participated in this study. The main outcome measures were live birth rate per first cycle of IVF differentiated for the major predictive factors. For male subfertility the delivery rate per cycle was significantly lower than unexplained subfertility, OR of 0.70 (95% CI 0.57-0.86); for tubal pathology, the delivery rate was slightly lower, OR = 0.86 (95% CI 0.70-1.01). Smoking was associated with a significantly lower delivery rate was slightly lower; for OR = 0.72 (95% CI 0.61-0.84) and a significantly higher abortion rate compared to non-smoking delivery rates of 21.4% and 16.4%, respectively (P=0.02). Women with a BMI of > or = 27 kg/m2 had a significantly lower delivery rate, with an OR of 0.67 (95% CI 0.48-0.94), compared with normal weight women (BMI > or = 20 and <27 kg/m2). Both smoking and overweight unfavourably affect the live birth rate after IVF. The devastating impact of smoking on the live birth rate in IVF treatment is comparable with an increase in female age of >10 years from age 20 to 30 years. Subfertile couples may improve the outcome of IVF treatment by lifestyle changes.

ESTIMATED RISKS OF RADON-INDUCED LUNG CANCER FOR DIFFERENT EXPOSURE PROFILES BASED ON THE NEW EPA MODEL

Radon is a naturally occurring radioactive gas. When inhaled, radon can cause mutations that lead to lung cancer. Some new epidemiologic studies indicate that indoor radon is a public health problem. The BEIR VI report outlined its preferred two risk models for the combined effects of smoking and exposure to radon progeny, and listed the estimated risk to ever-smokers and never-smokers of both sexes due to lifetime exposure. However, exposures for shorter periods of time are of practical interest since exposure to elevated levels of radon may occur and end at any age. This study aims to produce practical tables of lifetime relative risks for exposures between any two age intervals from 0 to 110, and for various radon concentrations found in homes from 100 to 1,000 Bq m(-3). The calculations are based on the risk model developed recently by U.S. Environmental Protection Agency. The EPA's risk model is a single model that gives risk values midway between those obtained from the two BEIR VI preferred models. The detailed tables provide a clearer view of the age groups at higher risk and the effect of exposure duration. The results will help radiation protection practitioners to better communicate indoor radon risk to members of the public.

Combined effects of smoking and hypercholesterolemia on inflammatory process, thrombosis/fibrinolysis system, and forearm hyperemic response

The combined effects of smoking and hypercholesterolemia on the inflammatory process, the thrombosis/fibrinolysis system, and forearm hyperemic response were investigated. It was shown that smokers with hypercholesterolemia (n = 25) had a reduced and delayed forearm hyperemic response compared with healthy smokers (n = 24), patients with hypercholesterolemia (n = 26), and healthy controls (n = 75; p <0.01 for all). This phenomenon was associated with a respective increase in the inflammatory process and changes in the thrombosis/fibrinolysis system.

Haptoglobin 2-2 phenotype is associated with decreased ferroxidase activity in smokers

Background: Cigarette smoking and the inheritance of Hp 2-2 phenotype have been separately linked to cardiovascular disease. In this study, the combined effects of smoking and the presence of Hp 2-2 type on predisposition to cardiovascular disease were investigated. Methods: Fasting blood specimens were collected from 489 Jordanian males (228 smokers and 261 nonsmokers). Haptoglobin phenotype was determined by electrophoresis, and lipid profile and ferroxidase activity were determined by spectrophotometric methods. Results: The results show that, irrespective of Hp type, total- and LDL-cholesterol levels were significantly higher in smokers compared with nonsmokers, while levels of HDL-cholesterol and ferroxidase activity were lower in smokers. There was no significant difference between the three Hp types in nonsmokers regarding the lipid profile and ferroxidase activity. In the smokers group, however, serum ferroxidase activity was significantly lower in individuals with Hp 2-2 type compared with that in Hp 1-1 and Hp 2-1 smoker individuals. Smokers with the Hp 2-2 type have significantly higher levels of total- and LDL-cholesterol and lower HDL-cholesterol levels compared with that in nonsmokers expressing the same Hp type. Conclusion: These findings demonstrate that smokers with Hp 2-2 phenotype have a decreased antioxidant capacity suggesting that smoking coupled with the inheritance of an Hp-2-2 type predispose to more oxidative stress and cardiovascular disease.

Smoking while drinking coffee: a harmful, synergistic effect on arterial stiffness

Aortic stiffness is a prognosticator of cardiovascular risk and is involved in the pathogenesis of hypertension. We have shown that caffeine increases large artery stiffness. In contemporary lifestyle, the habitual consumption of caffeine is often associated with smoking; however, their combined effect on large artery stiffness has not been investigated. Caffeine led to a substantial increase in PWV (by 0.24 m/sec) and smoking increased further PWV (by 0.44 m/sec, left figure), an increase larger than that produced by smoking alone (by 0.34 m/sec, right figure). Pressures increased (systolic: by 16.8 with caffeine and by an additional 7.5 mmHg with smoking; diastolic: by 10.8 with caffeine and by an additional 5.1 mmHg with smoking). Smoking and caffeine have a synergistic adverse effect on arterial stiffness. This finding has important implications for pulsatile load of the heart and provides new insights into the combined effects of smoking and caffeine on the cardiovascular system.

Acute effects of cigarette smoking on cerebral oxygenation and hemodynamics: A combined study with near-infrared spectroscopy and transcranial Doppler sonography

Cigarette smoking has been shown to increase cerebral blood flow velocity (CBFV) and reduce vasomotor reactivity temporarily. The aim of our study was to clarify whether this results from dilation of resistance vessels alone with subsequent increase in regional cerebral blood flow (rCBF), or an additional constriction of basal cerebral arteries. In 24 healthy smokers (mean age±S.D., 32.7±10.5 years), cerebral oxygenation and hemodynamics were monitored by transcranial Doppler sonography and near-infrared spectroscopy before, during, and after smoking a cigarette (nicotine 0.9 mg). We simultaneously recorded CBFV of both middle cerebral arteries, mean arterial blood pressure, skin blood flow, end-tidal CO 2, changes in concentration of cerebral oxyhemoglobin, deoxyhemoglobin, and total hemoglobin (μmol/l), and a cerebral tissue oxygenation index. Smoking increased CBFV ( p<0.01), oxyhemoglobin ( p<0.01), and total hemoglobin ( p<0.01). After smoking, the increase in CBFV and total hemoglobin persisted ( p<0.01), while oxyhemoglobin returned to baseline. Deoxyhemoglobin and cerebral tissue oxygenation index did not change during the whole procedure. During, but not after smoking, CBFV increase was correlated to ipsilateral changes in oxyhemoglobin and total hemoglobin ( p<0.05). The increase in oxyhemoglobin only during smoking and the lack of changes in deoxyhemoglobin and cerebral tissue oxygenation index indicate that smoking did not substantially increase rCBF. The smoking-induced elevation in CBFV might therefore be due to an additional constriction of the middle cerebral artery. The combined effects of smoking on basal cerebral arteries and arterioles might contribute to the increased stroke risk in smokers.

Caffeine Intake and Fecundability: A Follow-up Study among 430 Danish Couples Planning Their First Pregnancy

Fecundability has been defined as the ability to achieve a recognized pregnancy. Several studies on caffeine and fecundability have been conducted but have been inconclusive. This may be explained partly by lack of stratification by smoking. Furthermore, few researchers have tried to separate the effect of caffeine from different sources (coffee, tea, cola, and chocolate). Clearly, the relationship between caffeine and fecundability needs further research, given the high prevalence of caffeine intake among women of childbearing age. We examined the independent and combined effects of smoking and caffeine intake from different sources on the probability of conception. From 1992 to 1995, a total of 430 couples were recruited after a nationwide mailing of a personal letter to 52,255 trade union members who were 20 to 35 years old, lived with a partner, and had no previous reproductive experience. At enrollment and in six cycles of follow-up, both partners filled out a questionnaire on different factors including smoking habits and their intake of coffee, tea, chocolate, cola beverages, and chocolate bars. In all, 1596 cycles and 423 couples were included in the analyses. The cycle-specific association between caffeine intake and fecundability was analyzed in a logistic regression model with the outcome at each cycle (pregnant or not pregnant) in a Cox discrete model calculating the fecundability odds-ratio (FR). Compared to nonsmoking women with caffeine intake less than 300 mg/d, nonsmoking women who consumed 300 to 700 mg/d caffeine had a FR of 0.88 [95% confidence interval (CI) 0.60–1.31], whereas women with a higher caffeine intake had a FR = 0.63 (95% CI 0.25–1.60) after adjusting for female body mass index and alcohol intake, diseases of the female reproductive organs, semen quality, and duration of menstrual cycle. No dose–response relationship was found among smokers. Among males, the same decline in point estimates of the FR was present. Smoking women whose only source of caffeine was coffee (>300 mg/d) had a reduced fecundability odds-ratio (FR = 0.34; 95% CI 0.12–0.98). An interaction between caffeine and smoking is biologically plausible, and the lack of effect among smokers may be due to faster metabolism of caffeine. Our findings suggest that especially nonsmoking women who wish to achieve a pregnancy might benefit from a reduced caffeine intake.

Smokers with IDDM experience excess morbidity. The Colorado IDDM Registry.

OBJECTIVE--To determine whether there is an association between smoking and the self-reported morbidity of people with IDDM and to evaluate the nature of a possible interaction between smoking and IDDM in increasing the risk of morbidity among smokers with IDDM. RESEARCH DESIGN AND METHODS--Subjects were non-Hispanic whites aged 18-28 yr who participated in the Colorado IDDM Registry Follow-up Survey (case subjects, n = 24) or the 1985 NHIS (control subjects, n = 5876). Assessments of self-reported morbidity included any hospitalization in the past year; bed days, sick days, and limited-activity days in the past 2 wk; and ratings of poor health. The criteria outlined by Saracci were used to determine whether smoking was associated with greater morbidity among IDDM case compared to control subjects (smoking by IDDM interaction). RESULTS--Age- and sex-adjusted ORs, estimated from logistic regression, showed that people with IDDM reported excess morbidity compared with control subjects, regardless of smoking status. Smokers with IDDM reported morbidity 3-10 times as often as nonsmoking control subjects and were 2-3 times more likely to report morbidity than nonsmokers with IDDM. The smoking by IDDM interaction was more than multiplicative for all morbidity measures. Fifty to 75% of excess morbidity in young smokers with IDDM over simple additive effects was related to the interaction between smoking and IDDM. CONCLUSIONS--There was excess reported morbidity among people with IDDM who smoked, greater than that expected from the combined effects of smoking and IDDM. Smoking cessation in young people with IDDM may alleviate some of this excess, but more study is needed to determine whether smoking serves as an indicator of poor IDDM care practices or has a physiological impact that compounds the morbidity experienced by people with IDDM.

Does asbestosis increase the risk of lung cancer?

The question of whether asbestos workers with or without asbestosis have the same risk of lung cancer has not been adequately addressed in the literature. Studies of asbestos workers indicate that clinical symptoms and abnormal lung X-rays are more frequent among smokers than non-smokers, and some studies show that workers with asbestosis compared to those without asbestosis are more likely to be smokers or ex-smokers. Since smoking has a large affect on the risks of lung cancer, smoking habits should be considered when evaluating the risk of lung cancer among persons with and without asbestosis. Some studies show that the risk of lung cancer is higher for persons with asbestosis compared to persons without asbestosis, but none of these studies also considered the combined effects of smoking and asbestos exposure on the risk of lung cancer. It is unlikely that the higher risk of lung cancer to persons with asbestosis is only due to their higher prevalence of smoking. Some studies have suggested that asbestos workers with asbestosis may have a higher risk of lung cancer, but no definite conclusions can be drawn since dose-response relations were not evaluated. Further studies are needed to evaluate the interrelationships of smoking, asbestosis and the risk of lung cancer.