Although recent reviews have suggested active smoking to be a risk factor for breast cancer, the association with passive smoke exposure remains controversial. This risk association was explored in a large prospective study of women, the California Teachers Study.
Detailed lifetime information on passive smoke exposure by setting (home, work, or social) and by age of exposure were collected in 1997 from 57,523 women who were lifetime nonsmokers and had no history of breast cancer. In the ensuing decade, a total of 1,754 women were diagnosed with invasive breast cancer. Cox proportional hazards models were fit to estimate hazard ratios (HRs) and 95% confidence intervals (95% CI) associated with several lifetime passive smoke exposure metrics.
For all breast cancer, measures of higher lifetime passive smoking intensity and duration were associated with non-statistically significant HRs of 1.11 to 1.14. For postmenopausal women, HRs for lifetime low, medium and high cumulative exposure were 1.17 (95%CI 0.91, 1.49), 1.19 (95%CI 0.93, 1.53), and 1.26 (95% CI 0.99, 1.60). For women exposed in adulthood (age ≥20) risk was elevated at the highest level of cumulative exposure (HR=1.18, 95% CI 1.00, 1.40), primarily among postmenopausal women (HR=1.25, 95% CI 1.01, 1.56). A statistically significant dose response was detected when analysis was restricted to women with moderate to high levels of passive smoke exposure.
These results suggest that cumulative exposures to high levels of side stream smoke may increase breast cancer risk among postmenopausal women who themselves have never smoked tobacco products.
passive smoking; tobacco; breast cancer; cohort study; women
Smoking, alcohol use, and obesity appear to increase the risk of developing non-Hodgkin lymphoma (NHL), but few studies have assessed their impact on NHL prognosis.
We evaluated the association of pre-diagnosis cigarette smoking, alcohol use, and body mass index (BMI) on overall survival in 1,286 patients enrolled through population-based registries in the United States from 1998–2000. Hazard Ratios (HR) and 95% confidence intervals (CI) were estimated using Cox regression, adjusting for clinical and demographic factors.
Through 2007, 442 patients died (34%), and the median follow-up on living patients was 7.7 years. Compared to never smokers, former (HR=1.59; 95% CI 1.12–2.26) and current (HR=1.50; 95% CI 0.97–2.29) smokers had poorer survival, and poorer survival was positively associated with smoking duration, number of cigarettes smoked per day, pack-years of smoking, and shorter time since quitting (all p-trend<0.01). Alcohol use was associated with poorer survival (p-trend=0.03); compared to non-users, those drinking more than 43.1 grams/week (median of intake among drinkers) had poorer survival (HR=1.55; 95% CI 1.06–2.27) while those drinkers consuming less than this amount showed no survival disadvantage (HR=1.13; 95% CI 0.75–1.71). Greater body mass index was associated with poorer survival (p-trend=0.046), but the survival disadvantage was only seen among obese individuals (HR=1.32 for BMI ≥30 versus 20–24.9 kg/m2; 95% CI 1.02–1.70). These results held for lymphoma-specific survival and were broadly similar for DLBCL and follicular lymphoma.
NHL patients who smoked, consumed alcohol or were obese prior to diagnosis had a poorer overall and lymphoma-specific survival.
alcohol; non-Hodgkin lymphoma; obesity; smoking; survival
We examined oral contraceptive (OC) and menopausal hormonal therapy (MHT) use in relation to risk of B-cell non-Hodgkin lymphoma (NHL). Women under age 85 years participating in the California Teachers Study with no history of hematopoietic cancer were followed from 1995 through 2007. 516 of 114,131 women eligible for OC use analysis and 402 of 54,758 postmenopausal women eligible for MHT use analysis developed B-cell NHL. Multivariable adjusted and stratified Cox proportional hazards models were fit to estimate relative risks (RR) and 95% confidence intervals (95% CI). Ever versus never OC use was marginally associated with lower B-cell NHL risk, particularly among women first using OCs before age 25 years (RR=0.72, 95%CI=0.51-0.99); yet, no duration-response effect was observed. No association was observed for ever versus never MHT use among postmenopausal women (RR=1.05, 95%CI=0.83-1.33) overall, or by formulation (estrogen alone, ET, or estrogen plus progestin, EPT). Among women with no MHT use, having bilateral oophorectomy plus hysterectomy was associated with greater B-cell NHL risk than having natural menopause (RR=3.15, 95%CI=1.62-6.13). Bilateral oophorectomy plus hysterectomy was not associated with risk among women who used ET or EPT. These results indicate that exogenous hormone use does not strongly influence B-cell NHL risk.
non-Hodgkin lymphoma; oral contraceptives; menopausal hormonal therapy; hysterectomy; bilateral oophorectomy
Non-Hodgkin lymphoma (NHL) is a malignancy etiologically linked to immunomodulatory exposures and disorders. Endogenous female sex hormones may modify immune function and influence NHL risk. Few studies have examined associations between reproductive factors, which can serve as surrogates for such hormonal exposures, and NHL risk by subtype.
Women in the California Teachers Study cohort provided detailed data in 1995–1996 on reproductive history. Follow-up through 2007 identified 574 women with incident B-cell NHL. Hazard rate ratios (RR) and 95% confidence intervals (CI) were estimated using Cox proportional hazards models to assess associations between reproductive factors and all B-cell NHL combined, diffuse large B-cell lymphomas, follicular lymphomas, and B-cell chronic lymphocytic leukemias/small lymphocytic lymphomas. Pregnancy was marginally associated with lower risk of B-cell NHL (RR = 0.84, 95% CI = 0.68–1.04). Much of the reduction in risk was observed after one full-term pregnancy relative to nulligravid women (RR = 0.75, 95% CI = 0.54–1.06; P for trend <0.01), particularly for diffuse large B-cell lymphomas (P for trend = 0.13), but not among women who had only incomplete pregnancies. Age at first full-term pregnancy was marginally inversely associated with B-cell NHL risk overall (P for trend = 0.08) and for diffuse large B-cell lymphomas (P for trend = 0.056). Breast feeding was not associated with B-cell NHL risk overall or by subtype.
Full-term pregnancy and early age at first full-term pregnancy account for most of the observed reduction in B-cell NHL risk associated with gravidity. Pregnancy-related hormonal exposures, including prolonged and high-level exposure to progesterone during a full-term pregnancy may inhibit development of B-cell NHL.
STUDY OBJECTIVES--To investigate the effects of passive exposure to tobacco smoke and gas cooking at home on respiratory symptoms and lung function of non-smoking women. SETTING--Evidence on the effects of passive smoking and exposure to nitrogen dioxide from gas cooking on the respiratory health of adults is limited and variable. Over 97% of women in Singapore do not smoke, and a principal source of indoor air pollution for housewives is passive smoking and gas cooking. DESIGN--This was a cross sectional (prevalence) study of a population based sample of 2868 adults aged 20 to 74 years in Singapore. A structured questionnaire administered by trained interviewers was used to collect data on passive smoking, gas cooking, respiratory symptoms, and other relevant variables. Passive smoking was defined as exposure to cigarette smoke from one or more members of the household who had ever smoked. Gas cooking was defined in terms of the weekly frequency of gas cooking, as well as the frequency with which the respondent's kitchen was filled with heavy cooking fumes (rarely, occasionally, often). Forced expiratory volume in one second (FEV1) was measured by using a portable Micro-spirometer. Multivariate analyses were used to estimate relative odds of association for respiratory symptoms and FEV1 effect, with adjustment for potential confounding variables. PARTICIPANTS--Of a total of 1438 women in the sample, 1282 women who had never smoked provided questionnaire data and 1008 women provided acceptable readings of FEV1 for analysis. MAIN RESULTS--Passive smoking was significantly associated with greater relative odds of usual or chronic cough and phlegm, wheezing, and breathlessness on exertion, as well as lower FEV1. Greater relative odds of respiratory symptoms were also associated with the weekly frequency of gas cooking, although these results were statistically insignificant. Chronic cough and phlegm and breathlessness on exertion, however, were significantly associated with the frequency with which the kitchen was filled with heavy cooking fumes. A lower FEV1 was found in women who cooked frequently (more than thrice a week). CONCLUSION--Domestic exposure to cigarette smoke and gas cooking is associated with increased risks of respiratory symptoms and impairment of lung function in non-smoking women in Singapore.
Parkinson disease is inversely associated with cigarette smoking, but its relation with passive smoking or environmental tobacco smoke exposure is rarely examined.
Within a case-control study we assessed the association between Parkinson disease and living or working with active smokers. Cases were newly diagnosed with idiopathic Parkinson disease (N=154) from western Washington State in 2002–2008. Age- and sex-matched controls (N=173) were neurologically normal and unrelated to cases.
Compared with never active or passive tobacco smokers, we observed similarly reduced Parkinson disease risks for ever passive smokers only (odds ratio=0.34, 95% confidence interval 0.16–0.73) as for ever active smokers (0.35, 0.17–0.73). Among persons whose only tobacco smoke exposure was passive smoking at home, risk was inversely associated with years exposed.
These observations parallel those well-established for active smoking. However, it remains unresolved whether a true protective effect of tobacco smoke, generally detrimental to health, underlies these associations.
Environmental Tobacco Smoke Pollution; Idiopathic Parkinson Disease; Passive Smoking; Smoking
Evidence links active cigarette smoking to cervical neoplasia, but much less is known about the role of passive smoking. Using a prospective cohort design, we examined personal cigarette smoking and household passive smoke exposure in relation to the risk of cervical neoplasia.
Cohorts were established based on data collected on the smoking status of all household members during private censuses of Washington County, Maryland in 1963 (n = 24,792) and 1975 (n = 26,381). Using the Washington County Cancer Registry, the occurrence of cervical neoplasia in the two cohorts was ascertained from 1963–1978 and from 1975–1994. Poisson regression models were fitted to estimate the relative risk of developing cervical neoplasia associated with active and passive smoking in both cohorts. The referent category for all comparisons was never smokers not exposed to passive smoking.
The adjusted relative risk and 95% confidence limits for passive smoking was 2.1 (1.3, 3.3) in the 1963 cohort and 1.4 (0.8, 2.4) in the 1975 cohort. The adjusted relative risk and 95% confidence limits for current smoking were 2.6 (1.7, 4.1) and 1.7 (1.1, 2.6) in the 1963 and 1975 cohort, respectively.
The associations were in the direction of increased risk for both passive smoking and current active smoking in both the 1963 and 1975 cohorts, but were stronger in the 1963 cohort. The results of this long-term, prospective cohort study corroborate the association between active cigarette smoking and cervical neoplasia and provide evidence that passive smoking is a risk factor for cervical neoplasia.
Active smoking has little or no effect on breast cancer risk but some investigators have suggested that passive smoking and its interaction with active smoking may be associated with an increased risk. In a population based case–control study of breast cancer in women aged 36–45 years at diagnosis, information on active smoking, passive smoking in the home, and other factors, was collected at interview from 639 cases and 640 controls. Women were categorised jointly by their active and passive smoking exposure. Among never smoking controls, women who also reported no passive smoking exposure were significantly more likely to be nulliparous and to be recent users of oral contraceptives. Among those never exposed to passive smoking, there was no significant association between active smoking and breast cancer, relative risk (RR) of 1.12 (95% confidence interval (CI) 0.72–1.73) for past smokers and RR of 1.19 (95% CI 0.72–1.95) for current smokers, nor was there an association with age started, duration or intensity of active smoking. Compared with women who were never active nor passive smokers, there was no significant association between passive smoking in the home and breast cancer risk in never smokers, RR of 0.89 (95% CI 0.64–1.25), in past smokers, RR of 1.09 (95% CI 0.75–1.56), or in current smokers, RR of 0.93 (95% CI 0.67–1.30). There was no trend with increasing duration of passive smoking and there was no heterogeneity among any of the subgroups examined. In this study, there was no evidence of an association between either active smoking or passive smoking in the home and risk of breast cancer.
breast cancer; smoking; passive smoking; case-control study
OBJECTIVE-To assess the risk of cardiorespiratory symptoms and mortality in non-smokers who were passively exposed to environmental smoke. DESIGN--Prospective study of cohort from general population first screened between 1972 and 1976 and followed up for an average of 11.5 years, with linkage of data from participants in the same household. SETTING--Renfrew and Paisely, adjacent burghs in urban west Scotland. SUBJECTS--15,399 Men and women (80% of all those aged 45-64 resident in Renfrew or Paisley) comprised the original cohort; 7997 attended for multiphasic screening with a cohabitee. Passive smoking and control groups were defined on the basis of a lifelong non-smoking index case and whether the cohabitee had ever smoked or never smoked. MAIN OUTCOME MEASURE--Cardiorespiratory signs and symptoms and mortality. RESULTS--Each of the cardiorespiratory symptoms examined produced relative risks greater than 1.0 (though none were significant) for passive smokers compared with controls. Adjusted forced expiratory volume in one second was significantly lower in passive smokers than controls. All cause mortality was higher in passive smokers than controls (rate ratio 1.27 (95% confidence interval 0.95 to 1.70)), as were all causes of death related to smoking (rate ratio 1.30 (0.91 to 1.85] and mortality from lung cancer (rate ratio 2.41 (0.45 to 12.83)) and ischaemic heart disease (rate ratio 2.01 (1.21 to 3.35)). When passive smokers were divided into high and low exposure groups on the basis of the amount smoked by their cohabitees those highly exposed had higher rates of symptoms and death. CONCLUSION--Exposure to environmental tobacco smoke cannot be regarded as a safe involuntary habit.
The objective of the present study was to examine the association between environmental tobacco smoke (ETS) and risk of lung cancer among never smokers, defined as subjects who smoked less than 100 cigarettes in their lifetime.
We conducted a population-based case–control study on lung cancer in Montreal, Canada (1996–2000) including 1,203 cases and 1513 controls. The present analysis is restricted to the 44 cases and 436 population controls who reported never smoking and completed the questionnaire on lifetime ETS exposure. Collected information included duration and intensity of exposure from multiple sources: inside home (parents, spouses, roommates and any other co-resident) and outside homes (in vehicles, social settings, and workplace). Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated between ETS and lung cancer, adjusting for age, sex, socioeconomic status (SES), and proxy respondent.
Overall there was no association between ETS cumulative exposure from all sources (measured in pack-years) and lung cancer: OR = 0.98 (95%CI: 0.40-2.38), comparing upper with lower tertiles of exposure. While there were no elevated ORs associated with ever having lived with parents who smoked (OR = 0.62; 95%CI: 0.32-1.21) or with spouses who smoked (OR = 0.39; 95%CI: 0.18-0.85), ETS exposure from sources outside homes was associated with a slight, although non-significant increased risk: OR = 2.30 (95%CI: 0.85-6.19) for the upper 50% exposed. There were no clear differences in ORs by age at exposure to ETS or by histologic type of tumour, though numbers of subjects in subgroup analyses were too small to provide reliable estimates.
No clear association between lifetime ETS exposure from all sources and increased risk of lung cancer was found in the current study.
Environmental tobacco smoke; Lung cancer; Case–control study
OBJECTIVES: To estimate the risk of ischaemic heart disease caused by exposure to environmental tobacco smoke and to explain why the associated excess risk is almost half that of smoking 20 cigarettes per day when the exposure is only about 1% that of smoking. DESIGN: Meta-analysis of all 19 acceptable published studies of risk of ischaemic heart disease in lifelong non-smokers who live with a smoker and in those who live with a non-smoker, five large prospective studies of smoking and ischaemic heart disease, and studies of platelet aggregation and studies of diet according to exposure to tobacco smoke. RESULTS: The relative risk of ischaemic heart disease associated with exposure to environmental tobacco smoke was 1.30 (95% confidence interval 1.22 to 1.38) at age 65. At the same age the estimated relative risk associated with smoking one cigarette per day was similar (1.39 (1.18 to 1.64)), while for 20 per day it was 1.78 (1.31 to 2.44). Two separate analyses indicated that non-smokers who live with smokers eat a diet that places them at a 6% higher risk of ischaemic heart disease, so the direct effect of environmental tobacco smoke is to increase risk by 23% (14% to 33%), since 1.30/1.06 = 1.23. Platelet aggregation provides a plausible and quantitatively consistent mechanism for the low dose effect. The increase in platelet aggregation produced experimentally by exposure to environmental tobacco smoke would be expected to have acute effects increasing the risk of ischaemic heart disease by 34%. CONCLUSION: Breathing other people's smoke is an important and avoidable cause of ischaemic heart disease, increasing a person's risk by a quarter.
OBJECTIVE—To estimate the relative risk of stroke associated with exposure to environmental tobacco smoke (ETS, passive smoking) and to estimate the risk of stroke associated with current smoking (active smoking) using the traditional baseline group (never-smokers) and a baseline group that includes lifelong non-smokers and long-term (>10 years) ex-smokers who have not been exposed to ETS.
DESIGN AND SETTING—Population-based case-control study in residents of Auckland, New Zealand.
SUBJECTS—Cases were obtained from the Auckland stroke study, a population-based register of acute stroke. Controls were obtained from a cross-sectional survey of major cardiovascular risk factors measured in the same population. A standard questionaire was administered to patients and controls by trained nurse interviewers.
RESULTS—Information was available for 521 patients with first-ever acute stroke and 1851 community controls aged 35-74 years. After adjusting for potential confounders (age, sex, history of hypertension, heart disease, and diabetes) using logistic regression, exposure to ETS among non-smokers and long-term ex-smokers was associated with a significantly increased risk of stroke (odds ratio (OR) = 1.82; 95% confidence interval (95% CI) = 1.34 to 2.49). The risk was significant in men (OR = 2.10; 95% CI = 1.33 to 3.32) and women (OR = 1.66; 95% CI = 1.07 to 2.57). Active smokers had a fourfold risk of stroke compared with people who reported they had never smoked cigarettes (OR = 4.14; 95% CI = 3.04 to 5.63); the risk increased when active smokers were compared with people who had never smoked or had quit smoking more than 10 years earlier and who were not exposed to ETS (OR = 6.33; 95% CI = 4.50 to 8.91).
CONCLUSIONS—This study is one of the few to investigate the association between passive smoking and the risk of acute stroke. We found a significantly increased risk of stroke in men and in women. This study also confirms the higher risk of stroke in men and women who smoke cigarettes compared with non-smokers. The stroke risk increases further when those who have been exposed to ETS are excluded from the non-smoking reference group. These findings also suggest that studies investigating the adverse effects of smoking will underestimate the risk if exposure to ETS is not taken into account.
Keywords: environmental tobacco smoke; stroke; smoking-attributable diseases
Objective To assess whether active and passive smokers are more likely than non-smokers to develop clinically relevant glucose intolerance or diabetes.
Design Coronary artery risk development in young adults (CARDIA) is a prospective cohort study begun in 1985-6 with 15 years of follow-up.
Setting Participants recruited from Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California, USA.
Participants Black and white men and women aged 18-30 years with no glucose intolerance at baseline, including 1386 current smokers, 621 previous smokers, 1452 never smokers with reported exposure to secondhand smoke (validated by serum cotinine concentrations 1-15 ng/ml), and 1113 never smokers with no exposure to secondhand smoke.
Main outcome measure Time to development of glucose intolerance (glucose ≥ 100 mg/dl or taking antidiabetic drugs) during 15 years of follow-up.
Results Median age at baseline was 25, 55% of participants were women, and 50% were African-American. During follow-up, 16.7% of participants developed glucose intolerance. A graded association existed between smoking exposure and the development of glucose intolerance. The 15 year incidence of glucose intolerance was highest among smokers (21.8%), followed by never smokers with passive smoke exposure (17.2%), and then previous smokers (14.4%); it was lowest for never smokers with no passive smoke exposure (11.5%). Current smokers (hazard ratio 1.65, 95% confidence interval 1.27 to 2.13) and never smokers with passive smoke exposure (1.35, 1.06 to 1.71) remained at higher risk than never smokers without passive smoke exposure after adjustment for multiple baseline sociodemographic, biological, and behavioural factors, but risk in previous smokers was similar to that in never smokers without passive smoke exposure.
Conclusion These findings support a role of both active and passive smoking in the development of glucose intolerance in young adulthood.
Objective To measure the relation between environmental tobacco
smoke, as estimated by smoking in spouses, and long term mortality from
tobacco related disease.
Design Prospective cohort study covering 39 years.
Setting Adult population of California, United States.
Participants 118 094 adults enrolled in late 1959 in the American
Cancer Society cancer prevention study (CPS I), who were followed until 1998.
Particular focus is on the 35 561 never smokers who had a spouse in the study
with known smoking habits.
Main outcome measures Relative risks and 95% confidence intervals
for deaths from coronary heart disease, lung cancer, and chronic obstructive
pulmonary disease related to smoking in spouses and active cigarette
Results For participants followed from 1960 until 1998 the age
adjusted relative risk (95% confidence interval) for never smokers married to
ever smokers compared with never smokers married to never smokers was 0.94
(0.85 to 1.05) for coronary heart disease, 0.75 (0.42 to 1.35) for lung
cancer, and 1.27 (0.78 to 2.08) for chronic obstructive pulmonary disease
among 9619 men, and 1.01 (0.94 to 1.08), 0.99 (0.72 to 1.37), and 1.13 (0.80
to 1.58), respectively, among 25 942 women. No significant associations were
found for current or former exposure to environmental tobacco smoke before or
after adjusting for seven confounders and before or after excluding
participants with pre-existing disease. No significant associations were found
during the shorter follow up periods of 1960-5, 1966-72, 1973-85, and
Conclusions The results do not support a causal relation between
environmental tobacco smoke and tobacco related mortality, although they do
not rule out a small effect. The association between exposure to environmental
tobacco smoke and coronary heart disease and lung cancer may be considerably
weaker than generally believed.
Objective To explore the accounts of smokers and non-smokers (who live with smokers) of smoking in their homes and cars after the Scottish smoke-free legislation; to examine the reported impact of the legislation on smoking in the home; and to consider the implications for future initiatives aimed at reducing children's exposure to secondhand smoke in the home.
Design and setting A qualitative cross sectional study involving semistructured interviews conducted across Scotland shortly after the implementation of the legislation on 26 March 2006.
Participants A purposively selected sample of 50 adults (aged 18-75) drawn from all socioeconomic groups, included smokers living with smokers, smokers living with non-smokers, and non-smokers living with smokers.
Results Passive smoking was a well recognised term. Respondents had varied understandings of the risks of secondhand smoke, with a few rejecting evidence of such risks. Children, however, were perceived as vulnerable. Most reported that they restricted smoking in their homes, with a range of restrictions across social classes and home smoking profiles. Spatial, relational, health, and aesthetic factors influenced the development of restrictions. Children and grandchildren were important considerations in the development and modification of restrictions. Other strategies were also used to militate against secondhand smoke, such as opening windows. The meaning of the home as somewhere private and social identity were important underlying factors. Respondents reported greater restrictions on smoking in their cars. There were diverse views on the smoke-free legislation. Few thought it had influenced their smoking in the home, and none thought it had affected how they restricted smoking in their homes.
Conclusions These data suggest two normative discourses around smoking in the home. The first relates to acceptable social identity as a hospitable person who is not anti-smoker. The second relates to moral identity as a caring parent or grandparent. Awareness of the risks of secondhand smoke, despite ambivalence about health messages and the fluidity of smoking restrictions, provides clear opportunities for public health initiatives to support people attain smoke-free homes.
Epidemiological studies have consistently reported that active cigarette smoking is inversely associated with endometrial cancer risk. However, dose-response relationships with quantitative measures of active smoking or passive smoking remain less clear.
Data on lifetime active and passive smoking were collected for 551 endometrial cancer cases and 1925 controls in a population-based case-control study conducted during 2001–2003 in Poland (Warsaw and Łódz).
Compared with never active smokers, active current (Odds Ratio (OR)=0.51, 95% Confidence Interval (CI): 0.39, 0.68) and former smokers (OR=0.60, 95% CI: 0.45, 0.80) were at a statistically significantly decreased risk. We did not observe statistically significant inverse dose-response relationships with increasing exposure with duration and cumulative measures. However, there was some indication that the highest category of number of years (OR=0.35, 95% CI: 0.23–0.55), intensity (OR=0.41, 95% CI: 0.24–0.69), and dose (OR=0.38, 95% CI: 0.24–0.60) of smoking among current smokers had the greatest inverse association compared to never smokers. Our data did not support the presence of an inverse association with passive smoking among never active smokers (OR=0.92; 95% CI: 0.65, 1.29).
Our results support that long-term and heavy smoking among current smokers strongly influence endometrial cancer risk.
Endometrial cancer; Active smoking; Passive smoking
To assess the association between animal exposures and non-Hodgkin lymphoma (NHL).
Exposure data were collected from 1,591 cases and 2,515 controls during in-person interviews in a population-based case-control study of NHL in the San Francisco Bay Area. Odds ratios (ORs) and 95% confidence intervals (CIs) were adjusted for potential confounders.
Pet owners had a reduced risk of NHL (OR=0.71,CI=0.52 –0.97) and diffuse large-cell and immunoblastic large-cell (DLCL;OR=0.58,CI=0.39 –0.87) compared with those who never had owned a pet. Ever having owned dogs and/or cats was associated with reduced risk of all NHL (OR=0.71,CI=0.54–0.94) and of DLCL (OR=0.60,CI=0.42–0.86). Longer duration of cat ownership (p-trend=0.008), dog ownership (p-trend=0.04), and dog and/or cat ownership (p-trend =0.004) was inversely associated with risk of NHL. Ownership of pets other than cats and dogs was associated with a reduced risk of NHL (OR=0.64,CI=0.55–0.74) and DLCL (OR=0.58,CI=0.47 –0.71). Exposure to cattle for ≥5 years was associated with an increased risk of NHL (OR=1.6,CI=1.0–2.5) as was exposure to pigs for all NHL (OR=1.8,CI=1.2–2.6) and for DLCL (OR=2.0,CI=1.2–3.4).
The association between animal exposure and NHL warrants further investigation in pooled analyses.
lymphoma, non-Hodgkin; case-control; animal exposure; immunity; agricultural exposure
Active smoking is a well-established risk factor for myocardial infarction, but less is known about the impact of passive smoking, and possible sex differences in risk related to passive smoking. We investigated active and passive smoking as risk factors for myocardial infarction in an 11-year follow-up of 11,762 men and 13,206 women included in the Tromsø Study. There were a total of 769 and 453 incident cases of myocardial infarction in men and women, respectively. We found linear age-adjusted relationships between both active and passive smoking and myocardial infarction incidence in both sexes. The relationships seem to be stronger for women than for men. Age-adjusted analyses indicated a stronger relationship with passive smoking in ever-smokers than in never-smokers. After adjustment for important confounders (body mass index, blood pressure, total cholesterol, HDL cholesterol and physical activity) the associations with active and passive smoking were still statistically significant. Adjusting for active smoking when assessing the effect of passive smoking and vice versa, indicated that the effect of passive smoking in men may be explained by their own active smoking. In women, living with a smoker ≥30 years after the age of 20 increased the myocardial infarction risk by 40 %, even after adjusting for active smoking. Passive smoking is a risk factor for myocardial infarction on its own, but whereas the effect for men seems to be explained by their own active smoking, the effect in females remains statistically significant.
Cigarette smoking; Involuntary smoking; Passive smoking; Sex; Myocardial infarction
Studies of smoking and risk of non-Hodgkin lymphoma (NHL) have yielded inconsistent results, possibly due to subtype heterogeneity and/or genetic variation impacting the metabolism of tobacco-derived carcinogens, including substrates of the N-acetyltransferase enzymes NAT1 and NAT2.
We conducted a pooled analysis of 5,026 NHL cases and 4,630 controls from seven case–control studies in the international lymphoma epidemiology consortium to examine associations between smoking, variation in the N-acetyltransferase genes NAT1 and NAT2, and risk of NHL subtypes. Smoking data were harmonized across studies, and genetic variants in NAT1 and NAT2 were used to infer acetylation phenotype of the NAT1 and NAT2 enzymes, respectively. Pooled odds ratios (ORs) and 95 % confidence intervals (95 % CIs) for risk of NHL and subtypes were calculated using joint fixed effects unconditional logistic regression models.
Current smoking was associated with a significant 30 % increased risk of follicular lymphoma (n = 1,176) but not NHL overall or other NHL subtypes. The association was similar among NAT2 slow (OR 1.36; 95 % CI 1.07–1.75) and intermediate/rapid (OR 1.27; 95 % CI 0.95–1.69) acetylators (pinteraction = 0.82) and also did not differ by NAT1*10 allelotype. Neither NAT2 phenotype nor NAT1*10 allelotype was associated with risk of NHL overall or NHL subtypes.
The current findings provide further evidence for a modest association between current smoking and follicular lymphoma risk and suggest that this association may not be influenced by variation in the N-acetyltransferase enzymes.
Non-Hodgkin lymphoma; Gene environment interaction; Cigarette smoking; N-acetyltransferase; Follicular lymphoma
Nutritional status and physical activity are known to alter immune function, which may be relevant to lymphomagenesis. The authors examined body size measurements and recreational physical activity in relation to risk of B-cell non-Hodgkin lymphoma (NHL) in the prospective California Teachers Study. Between 1995 and 2007, 574 women were diagnosed with incident B-cell NHL among 121,216 eligible women aged 22–84 years at cohort entry. Multivariable-adjusted relative risks and 95% confidence intervals were estimated by fitting Cox proportional hazards models for all B-cell NHL combined and for the 3 most common subtypes: diffuse large B-cell lymphoma, follicular lymphoma, and B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma. Height was positively associated with risk of all B-cell NHLs (for >1.70 vs. 1.61–1.65 m, relative risk = 1.50, 95% confidence interval: 1.16, 1.96) and chronic lymphocytic leukemia/small lymphocytic lymphoma (relative risk = 1.93, 95% confidence interval: 1.09, 3.41). Weight and body mass index at age 18 years were positive predictors of B-cell NHL risk overall. These findings indicate that greater height, which may reflect genetics, early life immune function, infectious exposures, nutrition, or growth hormone levels, may play a role in NHL etiology. Adiposity at age 18 years may be more relevant to NHL etiology than that in later life.
body mass index; body size; cohort studies; exercise; hip; lymphoma, non-Hodgkin; waist-hip ratio
Ocular adnexal marginal zone B-cell lymphoma (OAMZL) has been associated with Chlamydophila psittaci, an infection that may be transmitted by carrier animals. However, it is still unclear whether exposure to animals affects the risk of OAMZL in comparison with other lymphoma histotypes. We therefore investigated the role of professional and/or domestic exposures to animals in the occurrence of OAMZL, as compared with other types of lymphoma.
A hospital-based case–control study was carried out on 43 consecutive OAMZL patients (cases) and 87 consecutive patients with nodal non-Hodgkin's lymphomas (NHLs; controls). Multiple logistic regression (MLR) odds ratios (ORs), and 95% confidence intervals (CIs) were used to estimate the association between exposures to animals and OAMZL risk.
A higher proportion of cases reported a lifetime exposure to household animals (79.1% vs 64.4% among controls), with a non-statistical significant MLR-OR of 2.18 (95% CI: 0.85–5.62). The OAMZL cases more frequently reported a history of occupation in breeding and/or slaughtering than controls (34.9% vs 6.9%), with an overall increased risk of 7.69 (95%CI: 2.65–22.34).
These results indicate that, compared with nodal NHLs, the risk of OAMZL is markedly increased by contact with animals, particularly by occupational exposures.
non-Hodgkin's lymphomas; ocular adnexal marginal zone B-cell lymphoma epidemiology; animal exposure; Chlamydophila psittaci
Several previous studies found inverse associations between alcohol consumption and risk of non-Hodgkin lymphoma (NHL) and multiple myeloma. However, most studies were retrospective, and few distinguished former drinkers or infrequent drinkers from consistent nondrinkers. Therefore, the authors investigated whether history of alcohol drinking affected risks of NHL and multiple myeloma among 102,721 eligible women in the California Teachers Study, a prospective cohort study in which 496 women were diagnosed with B-cell NHL and 101 were diagnosed with multiple myeloma between 1995–1996 and December 31, 2007. Incidence rate ratios and 95% confidence intervals were estimated using Cox proportional hazards regression. Risk of all types of B-cell NHL combined or multiple myeloma was not associated with self-reported past consumption of alcohol, beer, wine, or liquor at ages 18–22 years, at ages 30–35 years, or during the year before baseline. NHL subtypes were inconsistently associated with alcohol intake. However, women who were former alcohol drinkers at baseline were at elevated risk of overall B-cell NHL (rate ratio = 1.46, 95% confidence interval: 1.08, 1.97) and follicular lymphoma (rate ratio = 1.81, 95% confidence interval: 1.00, 3.28). The higher risk among former drinkers emphasizes the importance of classifying both current and past alcohol consumption and suggests that factors related to quitting drinking, rather than alcohol itself, may increase B-cell NHL risk.
alcohol drinking; cohort studies; lymphoma, non-Hodgkin; multiple myeloma
Objective To examine the association between smoking and risk of invasive breast cancer using quantitative measures of lifetime passive and active smoking exposure among postmenopausal women.
Design Prospective cohort study.
Setting 40 clinical centres in the United States.
Participants 79 990 women aged 50–79 enrolled in the Women’s Health Initiative Observational Study during 1993–8.
Main outcome measures Self reported active and passive smoking, pathologically confirmed invasive breast cancer.
Results In total, 3520 incident cases of invasive breast cancer were identified during an average of 10.3 years of follow-up. Compared with women who had never smoked, breast cancer risk was elevated by 9% among former smokers (hazard ratio 1.09 (95% CI 1.02 to 1.17)) and by 16% among current smokers (hazard ratio 1.16 (1.00 to 1.34)). Significantly higher breast cancer risk was observed in active smokers with high intensity and duration of smoking, as well as with initiation of smoking in the teenage years. The highest breast cancer risk was found among women who had smoked for ≥50 years or more (hazard ratio 1.35 (1.03 to1.77) compared with all lifetime non-smokers, hazard ratio 1.45 (1.06 to 1.98) compared with lifetime non-smokers with no exposure to passive smoking). An increased risk of breast cancer persisted for up to 20 years after smoking cessation. Among women who had never smoked, after adjustment for potential confounders, those with the most extensive exposure to passive smoking (≥10 years’ exposure in childhood, ≥20 years’ exposure as an adult at home, and ≥10 years’ exposure as an adult at work) had a 32% excess risk of breast cancer compared with those who had never been exposed to passive smoking (hazard ratio 1.32 (1.04 to 1.67)). However, there was no significant association in the other groups with lower exposure and no clear dose response to cumulative passive smoking exposure.
Conclusions Active smoking was associated with an increase in breast cancer risk among postmenopausal women. There was also a suggestion of an association between passive smoking and increased risk of breast cancer.
We examined whether dietary intake of isoflavones, lignans, isothiocyanates, antioxidants, or specific foods rich in these compounds is associated with reduced risk of B-cell non-Hodgkin lymphoma (NHL), multiple myeloma (MM), or Hodgkin lymphoma (HL) in a large, prospective cohort of women.
Between 1995-1996 and December 31, 2007, among 110,215 eligible members of the California Teachers Study cohort, 536 women developed incident B-cell NHL, 104 developed MM, and 34 developed HL. Cox proportional hazards regression, with age as the time-scale, was used to estimate adjusted rate ratios (RRs) with 95% confidence intervals (CIs) for risk of lymphoid malignancies.
Weak inverse associations with risk of diffuse large B-cell lymphoma were observed for isothiocyanates (RR for ≥12.1 vs. <2.7 mcM/day=0.67, 95% CI: 0.43-1.05) and an antioxidant index measuring hydroxyl radical absorbance capacity (RR for ≥2.2 vs. <0.9 μM Trolox equiv/g/day=0.68, 95% CI: 0.42-1.10; ptrend=0.08). Risk of other NHL subtypes, overall B-cell NHL, MM, or HL was not generally associated with dietary intake of isoflavones, lignans, isothiocyanates, antioxidants, or major food sources of these compounds.
Isoflavones, lignans, isothiocyanates, and antioxidant compounds are not associated with risk of most B-cell malignancies, but some phytocompounds may decrease risk of selected subtypes.
lymphoma; diet; isothiocyanates; antioxidants; cohort studies
It is now recognized that exposure to environmental tobacco smoke (ETS) in the workplace and other settings outside the home may be equally as important as residential ETS exposure. This review examines the sources of misclassification in the assessment of workplace ETS exposure in questionnaire-based epidemiologic studies. Cogent to this discussion is the role of misclassification of ever smokers as never smokers, which is important in studies of both workplace and residential ETS exposure and lung cancer and is discussed first. The collective evidence from studies that have used direct or indirect approaches to estimate smoker misclassification shows that although some misclassification of ever smokers as never smokers exists in studies of ETS and lung cancer, the potential bias from the misclassification of smokers is unlikely to explain the observed increased risk of lung cancer associated with ETS exposure.