Breast cancer and active and passive smoking: the role of the N-acetyltransferase 2 genotype

The association of breast cancer with passive and active smoking was investigated in slow and fast acetylators of aromatic amines in a Geneva, Switzerland, study in 1996-1997. A slow acetylator was homozygous for one, or heterozygous for two, of three N-acetyltransferase 2 (NAT2) polymorphisms determined on buccal cell DNA from 177 breast cancer cases and 170 age-matched, population controls. The reference group consisted of women never regularly exposed to active or passive smoke. Among premenopausal women, the odds ratios were homogeneous in slow and fast acetylators: 3.2 (95% confidence interval (CI): 1.2, 8.7) for passive smoking and 2.9 (95% CI: 1.1, 7.5) for active smoking. Among postmenopausal women, the odds ratios for fast acetylators were 11.6 (95% CI: 2.2, 62.2) for passive and 8.2 (95% CI: 1.4, 46.0) for active smoking; the corresponding effects were also apparent but less strong in slow acetylators. After the nonexposed and the passive smokers were grouped in a single reference category, active smoking was associated with postmenopausal breast cancer in slow acetylators (odds ratio (OR) = 2.5, 95% CI: 1.0, 6.2) but not in fast acetylators (OR = 1.3, 95% CI: 0.5, 3.3). Thus, the associations of both passive and active smoking with breast cancer appear stronger in fast than in slow NAT2 genotypes. Separating passive smokers from the nonexposed impacts on the inference about a possible NAT2-smoking interaction.     

Cigarette smoking and breast cancer.

An epidemiological case-control study was conducted in New York State, with 1617 primary breast cancer patients and an equal number of controls, to examine the relationship between cigarette smoking and breast cancer. Results showed no overall association between ever smokers versus never smokers and breast cancer risk (odds ratio [OR] = 1.03, 95% confidence interval [CI]: 0.90-1.19), nor was there any dose response trend observed with increased levels of smoking. In addition, no association was found with risk and age started smoking, age stopped smoking, amount smoked or total years smoked. Controlling for previously identified risk factors for breast cancer in the analysis did not significantly alter these relationships. Previous studies have found a difference in menopausal age among smokers compared to nonsmokers. The mean menopausal age was only slightly lower in smokers than in never smokers for both cases and controls. Breast cancer risk was observed to be close to unity for premenopausal women (OR = 0.97, 95% CI: 0.74-1.34) and postmenopausal women (OR = 1.06, 95% CI: 0.91-1.26). A recent study suggested breast cancer risk was more strongly related to starting smoking at a young age among women who smoked at least 25 or more cigarettes per day in the most recent year of smoking. This hypothesis was not supported by these data.     

Breast cancer and cigarette smoking: a hypothesis

In many studies, cigarette smoking has been associated with a small increase in breast cancer risk. The authors evaluated the relation of smoking to breast cancer risk in two case-control studies carried out from 1982 through 1986. In Canada, 607 women with breast cancer and 1,214 controls matched on decade of age and neighborhood were interviewed at home. In the United States, 1,955 cases of breast cancer and 805 controls with other cancers were interviewed in the hospital. In both studies, breast cancer risk was associated weakly with cigarette smoking overall. The odds ratio for women who had smoked 25 or more cigarettes per day as compared with never smokers was 1.2 (95% confidence interval (CI) 0.9-1.6) in the Canadian study and 1.2 (95% Cl 0.9-1.6) in the US study. In both studies, breast cancer risk was more strongly related to commencement of smoking at a young age. Among women who smoked at least 25 cigarettes per day in the most recent year of smoking, the odds ratios for commencement before age 16 years were 1.7 (95% Cl 1.0-2.9) in the Canadian data and 1.8 (95% Cl 1.0-3.4) in the US data, and the odds ratios for commencement at even younger ages were higher. The associations were not explained by duration of smoking, by the time elapsed since commencement, or by factors associated with cigarette smoking such as alcohol consumption or oral contraceptive use. Our findings raise the hypothesis that exposure to cigarette smoke during adolescence may increase a woman's risk of breast cancer. The hypothesis has biologic plausibility: cigarette smoke contains known carcinogens, and the developing breast is especially susceptible to cancer initiation.     

Cigarette smoking and the risk of breast cancer

The authors examined the relation between cigarette smoking and breast cancer in the Centers for Disease Control Cancer and Steroid Hormone Study, a multicenter, population-based case-control study. The study compared 4,720 women aged 20-54 years with newly diagnosed breast cancer identified through population-based tumor registries with 4,682 women randomly selected from the same geographic areas. Women who reported ever smoking cigarettes had a risk of breast cancer of 1.2 (95 percent confidence interval 1.1-1.3) compared with never smokers. There was no consistent dose-response pattern with any measure of smoking (pack-years of smoking, average number of cigarettes per day, or total years smoked) and little difference in risk between current and former smokers. There was some variation in risk by age, with slightly higher risk estimates for younger women than for older women. Although current smokers had an earlier natural menopause than did never smokers, the authors found no evidence of a protective effect of cigarette smoking on breast cancer risk. These findings suggest that the risk of breast cancer in women who smoke is the same as, or perhaps slightly higher than, women who have never smoked.     

Active smoking, passive smoking, and breast cancer risk: findings from the Japan Collaborative Cohort Study for Evaluation of Cancer Risk

Background

Evidence is lacking regarding the relationship between cigarette smoking and breast cancer in Japanese women. We examined the association between breast cancer incidence and active and passive smoking in the Japan Collaborative Cohort Study for Evaluation of Cancer Risk.

Methods

Our study comprised 34,401 women aged 40-79 years who had not been diagnosed previously with breast cancer and who provided information on smoking status at baseline (1988-1990). The subjects were followed from enrollment until December 31, 2001. Cox proportional-hazards models were used to estimate the hazard ratio (HR) and 95% confidence interval (CI) for the association between breast cancer incidence and tobacco smoke.

Results

During 271,412 person-years of follow-up, we identified 208 incident cases of breast cancer. Active smoking did not increase the risk of breast cancer, with a HR for current smokers of 0.67 (95% CI: 0.32-1.38). Furthermore, an increased risk of breast cancer was not observed in current smokers who smoked a greater number of cigarettes each day. Overall, passive smoking at home or in public spaces was also not associated with an increased risk of breast cancer among nonsmokers. Women who reported passive smoking during childhood had a statistically insignificant increase in risk (HR: 1.24; 95% CI: 0.84-1.85), compared with those who had not been exposed during this time.

Conclusion

Smoking may not be associated with an increased risk of breast cancer in this cohort of Japanese women.Key words: Smoking, Breast Neoplasms, Risk, Cohort Studies     

Active and passive smoking in breast cancer: prospective results from the Nurses' Health Study

BACKGROUND: The role of active and passive smoking in breast cancer remains controversial. METHODS: Using data collected in the prospective Nurses' Health Study, we examined the influence of active and passive smoking on the incidence of invasive breast cancer. The analysis was based on women responding to the 1982 questionnaire, which included questions on passive smoking exposure. Information on active smoking was collected in biennial questionnaires. A total of 78,206 women were followed prospectively from 1982 until June 1996. RESULTS: Of these women, 3,140 reported a diagnosis of invasive breast cancer during follow-up. Compared with never active smoking, relative risks (RR) of breast cancer were 1.04 (95% CI = 0.94-1.15) for current active smoking and 1.09 (95% CI = 1.00-1.18) for past active smoking. The RR for regular passive exposure at work and at home was 0.90 (95% CI = 0.67-1.22). For active smoking, a modest increase in risk was confined to women who began smoking before the age of 17 (RR = 1.19; 95% CI = 1.03-1.37). CONCLUSION: Results suggest that passive smoking is unrelated to breast cancer. However, results for active smoking are compatible with a small increase in risk when smoking is initiated at young ages.     

Active and passive cigarette smoke and breast cancer survival

PURPOSE: The association between active and passive cigarette smoking before breast cancer diagnosis and survival was investigated among a cohort of invasive breast cancer cases (n = 1273) participating in a population-based case-control study. METHODS: Participants diagnosed with a first primary breast cancer between August 1, 1996, and July 31, 1997, were followed-up until December 31, 2002, for all-cause mortality (n = 188 deaths), including breast cancer-specific mortality (n = 111), as reported to the National Death Index. RESULTS: In Cox models, the adjusted hazards ratios (HRs) for all-cause mortality were slightly higher among current and former active smokers, compared with never smokers (HR, 1.23; 95% confidence interval [95% CI], 0.83-1.84) and 1.19 (95% CI, 0.85-1.66), respectively). No association was found between active or passive smoking and breast cancer-specific mortality. All-cause and breast cancer-specific mortality was higher among active smokers who were postmenopausal (HR, 1.64; 95% CI, 1.03-2.60 and HR, 1.45; 95% CI, 0.78-2.70, respectively) or obese at diagnosis (HR, 2.10; 95% CI, 1.03-4.27 and HR, 1.97; 95% CI, 0.89-4.36, respectively). Associations between smoking and all-cause and breast cancer-specific mortality did not differ by cancer treatment. CONCLUSIONS: These data do not provide strong evidence for an association between smoking and all-cause or breast cancer-specific mortality, although smokers who are postmenopausal or obese at diagnosis may be at higher risk.     

Association of active and passive smoking with occupational injury in manual workers: a cross-sectional study of the 2011 Korean working conditions survey

This study was conducted to investigate the relationship of active and passive smoking with occupational injury among manual workers. Data from the 2011 Korean Working Conditions Survey were analyzed for 12,507 manual workers aged ≥15 yr. Overall, 60.4% of men and 5.8% of women were current smokers. The prevalence of injury was higher among never smokers who were exposed to secondhand smoke (SHS) (7.7% in men and 8.1% in women) than current smokers (4.2% in men and 4.1% in women). After controlling for potential confounders, in men, compared to those who never smoked and were not exposed to SHS, people who never smoked and were exposed to SHS (adjusted odds ratio (aOR)=3.7, 2.2–6.4) and current smokers (aOR=2.5, 1.6–3.8) were more likely to experience injury. Among women, the aORs of occupational injury were 8.4 (4.2–16.7) for never smoking women with occasional exposure to SHS and 3.5 (95% CI: 1.4–8.7) for current smokers, in comparison to never smoking women who were never exposed to SHS at work (reference group). The present study suggests that exposure to SHS is a possible risk factor of occupational injury for never smoking men and women.     

A prospective cohort study of bladder cancer risk in relation to active cigarette smoking and household exposure to secondhand cigarette smoke

Active cigarette smoking is a major risk factor for bladder cancer. Secondhand exposure to cigarette smoke may also contribute to bladder carcinogenesis. The authors conducted a prospective cohort study to examine the influence of both active smoking and household exposure to secondhand smoke (SHS) on subsequent bladder cancer risk. The study population included persons from two cohorts established from private censuses conducted in Washington County, Maryland, in 1963 (n = 45,749; 93 cases) and 1975 (n = 48,172; 172 cases). Poisson regression models were fitted to estimate the relative risk of bladder cancer associated with active and passive smoke exposure in the two cohorts (referent category: never smokers who did not live with any smokers). Current smokers had an elevated risk of bladder cancer in both the 1963 cohort (relative risk (RR) = 2.7, 95% confidence limits (CL): 1.6, 4.7) and the 1975 cohort (RR = 2.6, 95% CL: 1.7, 3.9) after adjustment for age, education, and marital status. Among nonsmoking women, current household SHS exposure was associated with bladder cancer risk in the 1963 cohort (RR = 2.3, 95% CL: 1.0, 5.4) but not in the 1975 cohort (RR = 0.9, 95% CL: 0.4, 2.3). This study further solidifies the evidence that active smoking is causally associated with bladder cancer. Additional studies are needed to determine whether passive smoking is a risk factor for bladder cancer.     

Cigarette smoking and increased risk of mucinous epithelial ovarian cancer

Several studies have reported that cigarette smoking is associated with an increased risk of mucinous ovarian cancer, but other studies have failed to find such a relation. Using data from the Case-Control Surveillance Study, begun in four US cities in 1976, the authors conducted a case-control study (1976-2001) to examine the association between cigarette smoking and the risk of ovarian cancer of different cell types. Among 709 incident cases of epithelial ovarian cancer, 402 were serous, 74 were mucinous, 106 were endometrioid, and 127 were of other cell types. For mucinous ovarian cancer, the odds ratios were 1.5 (95% confidence interval (CI): 0.7, 3.4) among women who smoked less than one pack of cigarettes per day, 1.4 (95% CI: 0.6, 3.5) among women who smoked one pack per day, and 2.9 (95% CI: 1.2, 7.5) among women who smoked more than one pack per day, relative to never smokers. The odds ratios were 2.5 (95% CI: 1.1, 5.4) for ex-smokers and 1.4 (95% CI: 0.7, 2.9) for current smokers. While women with up to 15 pack-years of smoking had an almost 2.5 times' increased risk of mucinous ovarian cancer, such an increased risk was not found among those with more than 15 pack-years of smoking. There was no association between cigarette smoking and epithelial ovarian cancer of other cell types. Despite inconsistencies in the data, these results strengthen the evidence that cigarette smoking may play a role in the development of mucinous ovarian cancer but not ovarian cancer of other cell types.     

Environmental tobacco smoke and breast cancer incidence

To evaluate whether environmental tobacco smoke (ETS) influences breast cancer incidence, data from a population-based case-control study were analyzed. Respondents with available ETS information assessed by in-person questionnaires included 1356 newly diagnosed cases and 1383 controls. Relative to nonsmokers who reported no residential ETS exposure throughout the life course, the odds ratios (OR) for breast cancer were not substantially elevated in relation to ETS exposure, active smoking, or a joint measure of active and passive smoking (OR, 1.15, 95% CI, 0.90, 1.48). An increased OR, however, was noted among nonsmokers who lived with a smoking spouse for over 27 years (2.10, 95% CI, 1.47, 3.02), although no dose-response was evident. Also, among women with hormone-receptor-positive tumors only, the OR for both active and passive smoking was increased (1.42 for ER+ PR+, 95% CI, 1.00, 2.00). Our data suggest that if there is an effect for ETS on breast cancer, that effect is restricted to selected subgroups of women, such as those with long-term exposure from a smoking spouse.     

Active and passive smoking and depression among Japanese workers

OBJECTIVE: To assess the relation of passive and active smoking to depressive symptoms in 1839 men and 931 women working in a suburb of Tokyo in 2002. METHOD: Self-reported smoking history and exposure to passive smoking (no, occasional, or regular) at work and at home. Depressive symptoms according to the Center for Epidemiologic Studies Depression Scale, with a cut-off point of 16. RESULTS: Compared to never smokers unexposed to passive smoking, never smokers reporting regular and occasional exposure to passive smoking at work had increased depressive symptoms. The adjusted odds ratios (aORs) were 1.92 (95% confidence interval (CI) 1.14, 3.23) for regular exposure and 1.63 (95% CI 1.08, 2.47) for occasional exposure. Current smokers had significantly increased depressive symptoms (aOR ranging from 2.25 to 2.38) but former smokers had only marginal increases of depressive symptoms (aOR ranging from 1.43 to 1.55). Gender did not modify the effects of active/passive smoking on depressive symptoms. CONCLUSION: Passive smoking at work and current smoking appear associated with higher levels of depressive symptoms.     

Active and passive smoking and risk of colds in women

PURPOSE: To evaluate the association between active and passive smoking and frequency of colds in women. METHODS: Data on cigarette smoking and frequency and duration of colds were analyzed in the Women's Health Study (WHS), a randomized, double-blind, placebo-controlled trial of low-dose aspirin and vitamin E in the primary prevention of cardiovascular disease and cancer among 39,876 female health professionals. RESULTS: After adjustment for age, body-mass index, prevalence of asthma and chronic lung diseases, alcohol intake, physical activity, and multivitamin use, current heavy smokers had no appreciable increase in the frequency of colds (relative risk (RR) for >or= 3 versus no colds in the past year, 1.05; 95% confidence interval (CI), 0.80-1.39), but a significantly increased risk of prolonged colds (RR for colds of > 7 vs. 1-3 days, 2.53; 95% CI, 1.95-3.29). There was no difference in the number of days confined to home. Nonsmoking women passively exposed to cigarette smoke had a slightly increased risk of both more frequent colds (RR, 1.33; 95% CI, 1.18-1.51) and more prolonged colds during the previous year (RR, 1.12; 95% CI, 0.99-1.27). CONCLUSIONS: Women who are currently heavy smokers are at increased risk of having colds with longer duration compared with nonsmokers. Nonsmoking women passively exposed to cigarette smoking are at slightly increased risk of having more frequent and longer colds than nonsmoking women not exposed to passive smoke.     

Associations of maternal prenatal smoking with child adiposity and blood pressure

OBJECTIVE: To examine the extent to which maternal prenatal smoking is associated with adiposity, central adiposity, and blood pressure in 3-year-old children. RESEARCH METHODS AND PROCEDURES: We studied 746 mother-child pairs in Project Viva, a prospective cohort study, and categorized mothers as never, early pregnancy, or former smokers. Main outcome measures were overweight (BMI for age and sex > 85th percentile), BMI z-score, sum of subscapular (SS) and triceps (TR) skinfolds, SS:TR skinfold ratio, and systolic blood pressure (SBP). RESULTS: One hundred sixty-one (22%) mothers quit smoking before pregnancy, 71 (10%) smoked in early pregnancy, and 514 (69%) never smoked. At age 3 years, 204 (27%) children were overweight. On multivariable analysis, compared with children of never smokers, children of early pregnancy smokers had an elevated risk for overweight [odds ratio (OR), 2.2; 95% confidence interval (CI), 1.2, 3.9] and higher BMI z-score (0.30 units; 95% CI, 0.05, 0.55), SS + TR (2.0 mm; 95% CI, 0.9, 3.0), and SBP (2.4 mm Hg; 95% CI, -0.1, 4.9). Children of former smokers were not more overweight (BMI z-score, 0.02 units; 95% CI, -0.15, 0.19) but had higher SBP (1.5 mm Hg; 95% CI, -0.1, 3.2). We saw no relationship of smoking with central adiposity (SS:TR). DISCUSSION: Former and early pregnancy smokers had children with somewhat higher SBP, but only early pregnancy smokers had children who were more overweight. Mechanisms linking smoking with child adiposity and blood pressure may differ. A long-term impact of maternal smoking on offspring cardiovascular risk provides further reason to reduce smoking in women.     

N-acetyltransferase 2 polymorphisms, tobacco smoking, and breast cancer risk in the breast and prostate cancer cohort consortium

Common polymorphisms in the N-acetyltransferase 2 gene (NAT2) modify the association between cigarette smoking and bladder cancer and have been hypothesized to determine whether active cigarette smoking increases breast cancer risk. The authors sought to replicate the latter hypothesis in a prospective analysis of 6,900 breast cancer cases and 9,903 matched controls drawn from 6 cohorts (1989-2006) in the National Cancer Institute's Breast and Prostate Cancer Cohort Consortium. Standardized methods were used to genotype the 3 most common polymorphisms that define NAT2 acetylation phenotype (rs1799930, rs1799931, and rs1801280). In unconditional logistic regression analyses, breast cancer risk was higher in women with more than 20 pack-years of active cigarette smoking than in never smokers (odds ratio (OR) = 1.28, 95% confidence interval (CI): 1.17, 1.39), after controlling for established risk factors other than alcohol consumption and physical inactivity. However, associations were similar for the slow (OR = 1.25, 95% CI: 1.11, 1.39) and rapid/intermediate (OR = 1.24, 95% CI: 1.08, 1.42) acetylation phenotypes, with no evidence of interaction (P = 0.87). These results provide some support for the hypothesis that long-term cigarette smoking may be causally associated with breast cancer risk but underscore the need for caution when interpreting sparse data on gene-environment interactions.     

Environmental tobacco smoke and the risk of pancreatic cancer: findings from a Canadian population-based case-control study

BACKGROUND: Despite the fact that tobacco is a well-recognized risk factor for pancreatic cancer, no study has yet reported on the association between environmental tobacco smoke (ETS) and this malignancy. We investigated the relationship between pancreatic cancer and childhood and adult exposure to ETS using a case-control study design. METHODS: Our study population consisted of 583 pancreatic cancer cases and 4,813 population-based controls that were identified within 8 Canadian provinces between 1994 and 1997. Mail-out questionnaires were used to collect risk factor information and a lifetime residential and occupational history of exposure to ETS. RESULTS: Among never smokers, those who were exposed to ETS both as a child and as an adult had an odds ratio of 1.21 (95% CI=0.60-2.44) relative to those with no exposure. For active smoking, when the referent group consisted of never smokers who had not been regularly exposed to ETS, the risk increases were more pronounced with an increased number of years of smoking, cigarette pack-years, years since quit smoking, and average number of cigarettes smoked daily. CONCLUSIONS: Overall, our results are suggestive of a weak association between pancreatic cancer and ETS. Perhaps more importantly, they suggest that ETS smoking exposures may confound the risk of pancreatic cancer associated with active smoking measures commonly used in epidemiologic studies.     

Active Smoking,Passive Smoking,and Risk of Nonalcoholic Fatty Liver Disease (NAFLD): A Population-Based Study in China

Background

The effect of active smoking on development of nonalcoholic fatty liver disease (NAFLD) is controversial, and there are limited clinical data on the relationship between passive smoking and NAFLD. We investigated whether active and passive smoking are associated with NAFLD.

Methods

A total of 8580 subjects (2691 men) aged 40 years or older participated in a community-based survey in Shanghai, China. Information on active and passive smoking was collected using a validated questionnaire. NAFLD was diagnosed by abdominal B-mode ultrasound testing and serum liver enzymes.

Results

NAFLD prevalence was 29.4% in never smokers, 34.2% in former smokers, 27.8% in light smokers (<20 cigarettes/day), 30.8% in moderate smokers (20–39 cigarettes/day), and 43.5% in heavy smokers (≥40 cigarettes/day). Fully adjusted logistic regression analyses revealed that, as compared with never smoking, former and heavy smoking were associated with increased risk of prevalent NAFLD, with odds ratios of 1.45 (95% CI 1.05–2.00) and 2.29 (95% CI 1.30–4.03), respectively. Active smoking and body mass index (BMI) had a synergistic effect on the risk of prevalent NAFLD; the combination of these risk factors was associated with the highest observed odds ratio for NAFLD: 8.58. In never-smoking women, passive smoking during both childhood and adulthood was associated with a 25% increase in the risk of prevalent NAFLD (OR = 1.25, 95% CI 1.05–1.50) as compared with no passive smoking.

Conclusions

Passive smoking and heavy active smoking are associated with prevalent NAFLD in middle-aged and elderly Chinese. Active smoking and BMI have a synergistic effect on prevalent NAFLD.Key words: active tobacco smoking, passive tobacco smoking, fatty liver     

Cigarette smoking and risk of breast carcinoma in situ

BACKGROUND: Although the associations with cigarette smoking have been explored extensively for invasive breast cancer, the relation to in situ cancer has not previously been examined in depth. METHODS: We analyzed data from a population-based case-control study of women living in Wisconsin, Massachusetts, and New Hampshire. Eligible cases of incident breast carcinoma in situ were reported to statewide registries in 1997-2001 (n = 1878); similarly aged controls (n = 8041) were randomly selected from population lists. Smoking history and other risk factor information were collected through structured telephone interviews. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated from logistic regression models adjusting for potential confounders. RESULTS: In multivariate models, the OR for breast carcinoma in situ among current smokers was 0.8, compared with never-smokers (95% CI = 0.7-1.0). Risk estimates increased towards the null with greater time since smoking cessation. Odds ratios were also less than 1.0 among women who initiated smoking in adolescence (OR = 0.8) or after a full-term birth (OR = 0.7), relative to women who never smoked. The reduced odds ratios associated with current smoking were strongest among women with annual screening mammograms (OR = 0.7; 95% CI = 0.6-0.9). Odds ratios were not less than 1.0 among current smokers without a recent screening mammogram (1.3; 0.9-2.0). CONCLUSIONS: Our findings suggest an inverse association between current smoking and risk of breast carcinoma in situ among women undergoing breast cancer screening.     

Antioxidant intake and risk of osteoporotic hip fracture in Utah: an effect modified by smoking status

The role of antioxidant intake in osteoporotic hip fracture risk is uncertain and may be modified by smoking. In the Utah Study of Nutrition and Bone Health, a statewide, population-based case-control study, the authors investigated whether antioxidant intake was associated with risk of osteoporotic hip fracture and whether this association was modified by smoking status. The analyses included data on 1,215 male and female cases aged > or = 50 years who incurred a hip fracture during 1997-2001 and 1,349 age- and sex-matched controls. Diet was assessed by food frequency questionnaire. Among ever smokers, participants in the highest quintile of vitamin E intake (vs. the lowest) had a lower risk of hip fracture after adjustment for confounders (odds ratio = 0.29, 95% confidence interval (CI): 0.16, 0.52; p-trend < 0.0001). The corresponding odds ratio for beta-carotene intake was 0.39 (95% CI: 0.23, 0.68; p-trend = 0.0004), and for selenium intake it was 0.27 (95% CI: 0.12, 0.58; p-trend = 0.0003). Vitamin C intake did not have a significant graded association with hip fracture risk among ever smokers. Similar findings were obtained when an overall antioxidant intake score was used (odds ratio = 0.19, 95% CI: 0.10, 0.37; p-trend < 0.0001). No similar associations were found in never smokers. Antioxidant intake was associated with reduced risk of osteoporotic hip fracture in these elderly subjects, and the effect was strongly modified by smoking status.     

Tobacco smoking in relation to pain in a national general population survey

BACKGROUND: We examined whether smoking status including heavy smoking (20 or more cigarettes per day) is related to the number of pain locations and intensity of pain. METHODS: A probability sample of the German national population aged 18 to 79 including 7124 participants (response proportion: 61.4%) was used. All individuals underwent a health examination between 1997 and 1999. Ordinal logistic regression analyses were performed with number of pain locations and pain intensity as dependent variables which had been assessed by questionnaire. RESULTS: Former and current heavy smokers had higher odds for greater numbers of pain locations and for moderate and intense pain than never smokers after adjustment for analgesic medicament use and behavior-related risk factors. Female former heavy smokers had an adjusted odds ratio (OR) of 1.6 (95% confidence interval, CI, 1.2-2.2) and male former heavy smokers had an adjusted OR of 1.4 (CI 1.1-1.8) for higher numbers of pain locations compared to never smoking women and men respectively (female current smokers: OR 1.4, CI 1.0-1.9; male current smokers: OR 1.3, CI 1.1-1.7). CONCLUSION: The findings suggest that former and current heavy smokers are more likely to report more pain locations and more intense pain than never smokers.