Mortality in relation to smoking: 22 years' observations on female British doctors.

A total of 6194 female doctors who in 1951 replied to a questionnaire about their smoking habits were followed up prospectively for 22 years. During that time 1094 died. Ischaemic heart disease, lung cancer, and chronic obstructive lung disease were all significantly (p < 0.001) related to smoking, though the absolute excess risks were lower than in male doctors smoking equivalent amounts. Female smokers born before the first world war were less likely to describe themselves as inhalers or as having started to smoke while young than were female smokers who were born later. In these respects this younger group resembled male smokers, and as they move into their 60s and 70s their absolute risk of lung disease and relative risk of ischaemic heart disease will probably come to resemble the risks for men smoking the same numbers of cigarettes. These findings show only that cigarette smoking causes lung cancer, chronic obstructive lung disease, and heart disease in women as in men. Whether the proportional increase in mortality from these diseases is as great in women as in men might be estimated directly from new case-control studies on men and women born since 1920.     

Follow up of New Zealand participants in British atmospheric nuclear weapons tests in the Pacific.

OBJECTIVE--To study the health of Royal New Zealand Navy personnel who participated in atmospheric nuclear weapons tests conducted by the United Kingdom at Malden Island and Christmas Island in 1957 and 1958. DESIGN--Blinded, controlled follow up of up to 30 years. SETTING--New Zealand. SUBJECTS--528 Men known to have participated in the tests and a control group of 1504 men who were in the Royal New Zealand Navy during the same period but did not participate in the tests. MAIN OUTCOME MEASURES--Mortality and incidence of cancer. RESULTS--Follow up for the period 1957-87 was 94% complete in test participants and 91% complete in the controls. There were 70 deaths among test participants and 179 deaths among controls, yielding a relative risk of 1.08 (90% confidence interval 0.85 to 1.38, p = 0.29). The relative risk of death from causes other than cancer was 0.96 (0.71 to 1.29, p = 0.59) whereas the relative risk of death from cancer was 1.38 (0.90 to 2.10, p = 0.09) and of the incidence of cancer was 1.12 (0.78 to 1.60, p = 0.29). For cancers other than haematological malignancies the relative risk was 1.14 (0.69 to 1.83, p = 0.31) for mortality and 1.01 (0.67 to 1.50, p = 0.48) for incidence. There were seven deaths from haematological cancers among test participants (relative risk 3.25, 90% confidence interval 1.12 to 9.64, p = 0.02), including four leukaemias (5.58, 1.04 to 41.6, p = 0.03). The relative risk for incidence of haematological cancers was 1.94 (0.74 to 4.84, p = 0.10) and that for leukaemia was 5.51 (1.03 to 41.1, p = 0.03). There were no cases of multiple myeloma in the test participants during the follow up period, but the expected number was only 0.3. CONCLUSIONS--Although the numbers are small, the findings for leukaemia are similar to those for British participants in the nuclear weapons test programme. Some leukaemias, and possibly some other haematological cancers, may have resulted from participation in this programme. There is little evidence of an increased risk for non-haematological cancers, and there is no evidence of an increased risk for causes of death other than cancer.     

Epipodophyllotoxins,alkylating agents,and radiation and risk of secondary leukaemia after childhood cancer.

OBJECTIVE--To investigate the incidence and aetiology of secondary leukaemia after childhood cancer in Britain. DESIGN--Cohort study and a case-control study. SETTING--Britain and population based National Register of Childhood Tumours. SUBJECTS--Cohort of 16,422 one year survivors of childhood cancer diagnosed in Britain between 1962 and 1983, among whom 22 secondary leukaemias were observed. A case-control study of 26 secondary leukaemias observed among survivors of childhood cancer diagnosed in Britain between 1940 and 1983; 96 controls were selected matched for sex, type of first cancer, age at first cancer, and interval to diagnosis of secondary leukaemia. MAIN OUTCOME MEASURES--Dose of radiation averaged over patients'' active bone marrow and total accumulated dose of epipodophyllotoxins, alkylating agents, vinca alkaloids, antimetabolites, and antibiotics (mg/m2) given for the original cancer. RESULTS--Cumulative risk of secondary leukaemia within the cohort did not exceed 0.5% over the initial five years beyond one year survival, except that after non-Hodgkin''s lymphomas 1.4% of patients developed secondary leukaemia. Corresponding figure for patients treated for non-Hodgkin''s lymphomas in the early 1980s was 4%. The relative risk of secondary leukaemia increased significantly with exposure to epipodophyllotoxins and dose of radiation averaged over patients'' active bone marrow. Ten patients developed leukaemia after having an epipodophyllotoxin-teniposide in nine cases, etoposide in one. Chromosomal translocations involving 11q23 were observed relating to two secondary leukaemias from a total of six for which there were successful cytogenetic studies after administration of an epipodophyllotoxin. CONCLUSIONS--Epipodophyllotoxins acting alone or together with alkylating agents or radiation seem to be involved in secondary leukaemia after childhood cancer.     

Body weight and mortality in middle aged British men: impact of smoking.

OBJECTIVE--To assess the relation between body mass index and mortality in middle aged British men. DESIGN--Men who were recruited for the British Regional Heart Study were followed up for a mean of nine years. SETTING--General practices in 24 British towns. SUBJECTS--7735 Men aged 40-59 years selected from the age-sex registers of one group practice in each of the 24 towns. MAIN OUTCOME MEASURE--Mortality from cardiovascular and non-cardiovascular causes. RESULTS--660 Of the men died. There was a U-shaped relation between body mass index and total mortality. Very lean men (less than 20 kg/m2) had by far the highest mortality followed by lean men (20-22 kg/m2) and obese men (greater than or equal to 28 kg/m2). The high mortality in lean and very lean men was due largely to non-cardiovascular causes, particularly lung cancer and respiratory disease, which are associated with cigarette smoking. In obese men deaths were more likely to be due to cardiovascular causes. There was a strong inverse association between body weight and cigarette smoking. When the pattern of mortality was examined by age, smoking habits, and pre-existing smoking related disease both very lean men and obese men consistently had an increased mortality. The U-shaped relation was most prominent in men in the oldest age group (55-59). Current smokers had a higher mortality than former smokers at virtually all values of body mass index. An increased mortality in lean men was seen only in current smokers and in men with smoking related disease. Among men who had never smoked, lean men had the lowest total mortality, thereafter mortality increased with increasing body mass index (p less than 0.01). CONCLUSIONS--This study provides strong evidence of the impact of cigarette smoking on body weight and mortality and strongly suggests that the benefits of giving up smoking are far greater than the problems associated with the increase in weight that may occur.     

Factors contributing to chromosome damage in lymphocytes of cigarette smokers

Cigarette smoking is generally believed to be responsible for a substantial number of human health problems. However, the causal relationship between smoking, the induction of biological effects and the extent of health problems among smokers have not been fully documented. Using the recently developed lymphocyte micronucleus (MN) assay, we have evaluated the chromosome aberration frequencies in 67 cigarette smokers and 59 matched non-smoking control subjects. We found that the mean MN frequency (per 100 cells) in the smokers was slightly higher than that found in the non-smokers (0.71 +/- 0.23 and 0.58 +/- 0.05 respectively; p less than 0.08). Factors which contribute to the expression of chromosome aberrations were also investigated. A significant age-dependent increase in MN frequencies was observed in both groups (p less than 0.05). Linear regression analysis showed that the age-dependent effects among smokers (r = 0.54; p less than 0.02) was further enhanced by cigarette consumption (r = 0.62; p less than 0.005). Consumption of low potency 'one-a-day' type multivitamins had no effect on MN frequencies in either sex of non-smokers and in the 1 male smoker who took multivitamins but vitamin intake consistently reduced the MN frequencies among female smokers. Using a challenge assay, fidelity of DNA repair was evaluated. Lymphocytes from both smokers and non-smokers were irradiated with single doses of 0 or 100 cGy of X-rays or with double doses of 100 cGy of X-rays each separated by 15 or 60 min (100/15 or 100/60). Chromosome translocation frequencies were consistently higher after irradiation in lymphocytes from smokers than in those from non-smokers. Statistically significant differences were detected when the cells were irradiated with the double doses of 100 cGy X-rays each separated by 60 min (p less than 0.05). These data suggest that lymphocytes from smokers made more mistakes in the repair of DNA damage than cells from non-smokers. Our studies provide new insights into the genotoxic effects of cigarette smoke and new information which may be useful for understanding the mechanisms for induction of health problems from smoking.     

Influence of sex,age, body mass index,and smoking on alcohol intake and mortality.

OBJECTIVE--To examine the association between self reported alcohol intake and subsequent mortality from all causes and if the effect of alcohol intake on the risk of death is modified by sex, age, body mass index, and smoking. DESIGN--Prospective population study with baseline assessment of alcohol and tobacco consumption and body mass index, and 10-12 years'' follow up of mortality. SETTING--Copenhagen city heart study, Denmark. SUBJECTS--7234 women and 6051 men aged 30-79 years. MAIN OUTCOME MEASURE--Number and time of deaths from 1976 to 1988. RESULTS--A total of 2229 people died, 1398 being men. A U shaped curve described the relation between alcohol intake and mortality. The lowest risk was observed at one to six alcoholic beverages a week (relative risk set at 1). Abstainers had a relative risk of 1.37 (95% confidence interval 1.20 to 1.56) whereas those drinking more than 70 beverages a week had a relative risk of 2.29 (1.75 to 3.00). Among the drinkers, the risk was significantly increased only among those drinking more than 42 beverages a week. Sex, age, body mass index, and smoking did not significantly modify the risk function. The risk among heavy drinkers was slightly reduced when smoking was controlled for. The risk function was similar in the first and second period of six years of observation. CONCLUSION--Alcohol intake showed a U shaped relation to mortality with the nadir at one to six beverages a week. The risk function was not modified by sex, age, body mass index, or smoking and remained stable over 12 years.     

Passive exposure to tobacco smoke: saliva cotinine concentrations in a representative population sample of non-smoking schoolchildren.

Saliva cotinine concentrations in 569 non-smoking schoolchildren were strongly related to the smoking habits of their parents. When neither parent smoked the mean concentration was 0.44 ng/ml, rising to 3.38 ng/ml when both parents were cigarette smokers. Mothers'' smoking had a stronger influence than did fathers'' (p less than 0.01). In addition, there was a small independent effect of number of siblings who smoked (p less than 0.01). The dose of nicotine received from fathers'' smoking was estimated as equivalent to the active smoking of 30 cigarettes a year, that from mothers'' smoking as equivalent to smoking 50 cigarettes a year, and that from both parents smoking as equivalent to smoking 80 cigarettes a year. This unsolicited burden may be prolonged throughout childhood and poses a definite risk to health.     

Mortality in relation to smoking: 40 years' observations on male British doctors.

OBJECTIVE--To assess the hazards associated with long term use of tobacco. DESIGN--Prospective study of mortality in relation to smoking habits assessed in 1951 and again from time to time thereafter, with causes sought of deaths over 40 years (to 1991). Continuation of a study that was last reported after 20 years'' follow up (1951-71). SUBJECTS--34,439 British male doctors who replied to a postal questionnaire in 1951, of whom 10,000 had died during the first 20 years and another 10,000 have died during the second 20 years. RESULTS--Excess mortality associated with smoking was about twice as extreme during the second half of the study as it had been during the first half. The death rate ratios during 1971-91 (comparing continuing cigarette smokers with life-long non-smokers) were approximately threefold at ages 45-64 and twofold at ages 65-84. The excess mortality was chiefly from diseases that can be caused by smoking. Positive associations with smoking were confirmed for death from cancers of the mouth, oesophagus, pharynx, larynx, lung, pancreas, and bladder; from chronic obstructive pulmonary disease and other respiratory diseases; from vascular diseases; from peptic ulcer; and (perhaps because of confounding by personality and alcohol use) from cirrhosis, suicide, and poisoning. A negative association was confirmed with death from Parkinson''s disease. Those who stopped smoking before middle age subsequently avoided almost all of the excess risk that they would otherwise have suffered, but even those who stopped smoking in middle age were subsequently at substantially less risk than those who continued to smoke. CONCLUSION--Results from the first 20 years of this study, and of other studies at that time, substantially underestimated the hazards of long term use of tobacco. It now seems that about half of all regular cigarette smokers will eventually be killed by their habit.     

Smoking and leanness: evidence for change in Finland.

Many studies have shown smokers to weigh less than non-smokers, which is plausible given the metabolic effects of cigarette smoke. The interrelation between smoking and relative body weight and its change over time were analysed by using data from Finnish population based surveys from 1982 and 1987. Among both men and women the inverse association between smoking and body mass index was clearly weakened between 1982 and 1987. In 1987 among men aged 25-44 smoking was positively related to body mass index. Moreover, the relation between smoking and waist to hip girth ratio was positive in both sexes at all ages. Years of smoking was nevertheless confirmed as a significant inverse predictor of relative weight. A cluster of unfavourable health habits, including high consumption of alcohol and saturated fats, especially emerged among younger smokers. This may have been due to different selection of smokers in Finland, where smoking increasingly seems to be a form of deviant or risk taking behaviour. It is concluded that at a population level the metabolic effects of smoking seem to be increasingly overridden by several other unfavourable health behaviours of smokers.     

A meta-analysis of cigarette smoking,bone mineral density and risk of hip fracture: recognition of a major effect.

OBJECTIVE: To determine the magnitude and importance of the relation between smoking, bone mineral density, and risk of hip fracture according to age. DESIGN: Meta-analysis of 29 published cross sectional studies reporting the difference in bone density in 2156 smokers and 9705 non-smokers according to age, and of 19 cohort and case-control studies recording 3889 hip fractures reporting risk in smokers relative to non-smokers. RESULTS: In premenopausal women bone density was similar in smokers and non-smokers. Postmenopausal bone loss was greater in current smokers than non-smokers, bone density diminishing by about an additional 2% for every 10 year increase in age, with a difference of 6% at age 80. In current smokers relative to non-smokers the risk of hip fracture was similar at age 50 but greater thereafter by an estimated 17% at age 60, 41% at 70, 71% at 80, and 108% at 90. These estimates of relative risk by age, derived directly from a regression analysis of the studies of smoking and hip fracture, were close to estimates using the difference in bone density between smokers and non-smokers and the association between bone density and risk of hip fracture. The estimated cumulative risk of hip fracture in women in England was 19% in smokers and 12% in non-smokers to age 85; 37% and 22% to age 90. Among all women, one hip fracture in eight is attributable to smoking. Limited data in men suggest a similar proportionate effect of smoking as in women. The association was not explained by smokers being thinner, younger at menopause, and exercising less nor by actions of smoking on oestrogen, but smoking may have a direct action on bone. CONCLUSIONS: Hip fracture in old age is a major adverse effect of smoking after the menopause. The cumulative excess bone loss over decades is substantial, increasing the lifetime risk of hip fracture by about half.     

Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98

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 smoking.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 1973-98.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.     

Short-term passive smoking causes endothelial dysfunction via oxidative stress in nonsmokers

Recent studies have shown that passive smoking impairs vascular endothelial function and induces oxidative stress in humans. However, in most of the previous human data regarding tobacco-induced pathophysiology, vascular endothelial dysfunction and oxidative stress have been separately assessed. This study was designed to determine the association between the acute effect of passive smoking on vascular endothelial function and in-vivo oxidative stress status. We studied 30 healthy male Japanese volunteers (32 +/- 7 years) including 15 habitual smokers and 15 nonsmokers. After baseline echocardiographic, hemodynamic recording, and blood sampling, subjects were exposed to passive smoking for 30 min. Endothelium-dependent vasodilation was measured by using % flow-mediated vasodilation (%FMD) of the brachial artery and plasma levels of 8-isoprostane was measured by enzyme immunoassay before and after the passive smoking exposure. Baseline %FMD was lower (4.3% +/- 1.2% vs. 10.9% +/- 3.1%, p < 0.001) and baseline plasma 8-isoprostane level was higher (41.5 +/- 5.8 pg/mL vs. 26.9 +/- 5.4 pg/mL, p < 0.001) in smokers than those in nonsmokers. The %FMD and 8-isoprostane level did not change after passive smoking in smokers. In nonsmokers, however, the %FMD decreased (to 5.0% +/- 1.9%, p < 0.001) and the 8-isoprostane level increased (to 37.8 +/- 9.6 pg/mL, p < 0.001) significantly after 30 min passive smoking exposure, equivalently to the levels of smokers. Sixty corrected samples before and after passive smoking exposure in all patients showed a significant negative correlation between the % FMD and the plasma 8-isoprostane levels (n = 60, r = -0.69, p < 0.001). Even 30 min of passive smoking rapidly impairs vascular endothelial function, which is associated with oxidative stress. Our data provide the pathophysiological insight for the recent epidemiological evidence about the increased risk of coronary heart disease among nonsmokers exposed to passive smoking.     

Non-smoking wives of heavy smokers have a higher risk of lung cancer: a study from Japan.

In a study in 29 health centre districts in Japan 91 540 non-smoking wives aged 40 and above were followed up for 14 years (1966-79), and standardised mortality rates for lung cancer were assessed according to the smoking habits of their husbands. Wives of heavy smokers were found to have a higher risk of developing lung cancer and a dose-response relation was observed. The relation between the husband''s smoking and the wife''s risk of developing lung cancer showed a similar pattern when analysed by age and occupation of the husband. The risk was particularly great in agricultural families when the husbands were aged 40-59 at enrolment. The husbands'' smoking habit did not affect their wives'' risk of dying from other disease such as stomach cancer, cervical cancer, and ischaemic heart disease. The risk of developing emphysema and asthma seemed to be higher in non-smoking wives of heavy smokers but the effect was not statistically significant. The husband''s drinking habit seemed to have no effect on any causes of death in their wives, including lung cancer. These results indicate the possible importance of passive or indirect smoking as one of the causal factors of lung cancer. They also appear to explain the long-standing riddle of why many women develop lung cancer although they themselves are non-smokers. These results also cast doubt on the practice of assessing the relative risk of developing lung cancer in smokers by comparing them with non-smokers.     

Reverse causality and confounding and the associations of overweight and obesity with mortality

Objective: To examine the effect of reverse causality and confounding on the association of BMI with all‐cause and cause‐specific mortality. Research Methods and Procedures: Data from two large prospective studies were used. One (a community‐based cohort) included 8327 women and 7017 men who resided in two Scottish towns at the time of the baseline assessment in 1972–1976; the other (an occupational cohort) included 4016 men working in the central belt of Scotland at the time of the baseline assessment in 1970–1973. Participants in both cohorts were ages 45 to 64 years at baseline; the follow‐up period was 28 to 34 years. Results: In age‐adjusted analyses that did not take account of reverse causality or smoking, there was no association between being overweight (BMI 25 to <30 kg/m²) and mortality, and weak to modest associations between obesity (BMI ≥30 kg/m²) and mortality. There was a strong association between smoking and lower BMI in women and men in both cohorts (all p < 0.0001). Among never‐smokers and with the first 5 years of deaths removed, overweight was associated with an increase in all‐cause mortality (relative risk ranging from 1.12 to 1.38), and obesity was associated with a doubling of risk in men in both cohorts (relative risk, 2.10 and 1.96, respectively) and a 60% increase in women (relative risk, 1.56). In both never‐smokers and current smokers, being overweight or obese was associated with important increases in the risk of cardiovascular disease. Discussion: These findings demonstrate that with appropriate control for smoking and reverse causality, both overweight and obesity are associated with important increases in all‐cause and cause‐specific mortality, and in particular with cardiovascular disease mortality.     

Does breathing other people's tobacco smoke cause lung cancer?

The available epidemiological studies of lung cancer and exposure to other people''s tobacco smoke, in which exposure was assessed by whether or not a person classified as a non-smoker lived with a smoker, were identified and the results combined. There were 10 case-control studies and three prospective studies. Overall, there was a highly significant 35% increase in the risk of lung cancer among non-smokers living with smokers compared with non-smokers living with non-smokers (relative risk 1.35, 95% confidence interval 1.19 to 1.54). Part of this increase was almost certainly caused by the misclassification of some smokers as non-smokers. As smokers, who are more likely to get lung cancer than non-smokers, tend to live with smokers this misclassification probably exaggerated the estimated increase in risk. Adjustment for this error reduced the estimate to 30% (relative risk 1.30), but as people who live with non-smokers may still be exposed to other people''s smoke this estimate was revised again to allow for the fact that a truly unexposed reference group was not used. The increase in risk among non-smokers living with smokers compared with a completely unexposed group was thus estimated as 53% (relative risk of 1.53). This analysis, and the fact that non-smokers breathe environmental tobacco smoke, which contains carcinogens, into their lungs and that the generally accepted view is that there is no safe threshold for the effect of carcinogens, leads to the conclusion that breathing other people''s tobacco smoke is a cause of lung cancer. About a third of the cases of lung cancer in non-smokers who live with smokers, and about a quarter of the cases in non-smokers in general, may be attributed to such exposure.     

Meta-analysis of relation between cigarette smoking and stroke.

There is a lack of consensus among studies on the possible risks of stroke from cigarette smoking; because of this a meta-analysis was conducted. All published data on the association were sought and the relative risk for each study obtained whenever possible. The pooled relative risks were calculated by using estimates of the precision of the individual relative risks to weight their contribution to the meta-analysis. Thirty two separate studies were analysed. The overall relative risk of stroke associated with cigarette smoking was 1.5 (95% confidence interval 1.4 to 1.6). Considerable differences were seen in relative risks among the subtypes: cerebral infarction 1.9, cerebral haemorrhage 0.7, and subarachnoid haemorrhage 2.9. An effect of age on the relative risk was also noted; less than 55 years 2.9, 55-74 years 1.8, and greater than or equal to 75 years 1.1. A dose response between the number of cigarettes smoked and relative risk was noted, and there was a small increased risk in women compared with men. Ex-smokers under the age of 75 seemed to retain an appreciably increased risk of stroke (1.5); for all ages the relative risk in ex-smokers was 1.2. The meta-analysis provides strong evidence of an excess risk of stroke among cigarette smokers. Stroke should therefore be added to the list of diseases related to smoking.     

Relationship between Smoking and Obesity: A Cross-Sectional Study of 499,504 Middle-Aged Adults in the UK General Population

Background

There is a general perception that smoking protects against weight gain and this may influence commencement and continuation of smoking, especially among young women.

Methods

A cross-sectional study was conducted using baseline data from UK Biobank. Logistic regression analyses were used to explore the association between smoking and obesity; defined as body mass index (BMI) >30kg/m². Smoking was examined in terms of smoking status, amount smoked, duration of smoking and time since quitting and we adjusted for the potential confounding effects of age, sex, socioeconomic deprivation, physical activity, alcohol consumption, hypertension and diabetes.

Results

The study comprised 499,504 adults aged 31 to 69 years. Overall, current smokers were less likely to be obese than never smokers (adjusted OR 0.83 95% CI 0.81-0.86). However, there was no significant association in the youngest sub-group (≤40 years). Former smokers were more likely to be obese than both current smokers (adjusted OR 1.33 95% CI 1.30-1.37) and never smokers (adjusted OR 1.14 95% CI 1.12-1.15). Among smokers, the risk of obesity increased with the amount smoked and former heavy smokers were more likely to be obese than former light smokers (adjusted OR 1.60, 95% 1.56-1.64, p<0.001). Risk of obesity fell with time from quitting. After 30 years, former smokers still had higher risk of obesity than current smokers but the same risk as never smokers.

Conclusion

Beliefs that smoking protects against obesity may be over-simplistic; especially among younger and heavier smokers. Quitting smoking may be associated with temporary weight gain. Therefore, smoking cessation interventions should include weight management support.     

Effect of smoking on complications in patients undergoing free TRAM flap breast reconstruction

Free pedicled transverse rectus abdominis myocutaneous (TRAM) flap breast reconstruction is often advocated as the procedure of choice for autogenous tissue breast reconstruction in high-risk patients, such as smokers. However, whether use of the free TRAM flap is a desirable option for breast reconstruction in smokers is still unclear. All patients undergoing breast reconstruction with free TRAM flaps at our institution between February of 1989 and May of 1998 were reviewed. Patients were classified as smokers, former smokers (patients who had stopped smoking at least 4 weeks before surgery), and nonsmokers. Flap and donor-site complications in the three groups were compared. Information on demographic characteristics, body mass index, and comorbid medical conditions was used to perform multivariate statistical analysis. A total of 936 breast reconstructions with free TRAM flaps were performed in 718 patients (80.9 percent immediate; 23.3 percent bilateral). There were 478 nonsmokers, 150 former smokers, and 90 smokers. Flap complications occurred in 222 (23.7 percent) of 936 flaps. Smokers had a higher incidence of mastectomy flap necrosis than nonsmokers (18.9 percent versus 9.0 percent; p = 0.005). Smokers who underwent immediate reconstruction had a significantly higher incidence of mastectomy skin flap necrosis than did smokers who underwent delayed reconstruction (21.7 percent versus 0 percent; p = 0.039). Donor-site complications occurred in 106 (14.8 percent) of 718 patients. Donor-site complications were more common in smokers than in former smokers (25.6 percent versus 10.0 percent; p = 0.001) or nonsmokers (25.6 percent versus 14.2 percent; p = 0.007). Compared with nonsmokers, smokers had significantly higher rates of abdominal flap necrosis (4.4 percent versus 0.8 percent; p = 0.025) and hernia (6.7 percent versus 2.1 percent; p = 0.016). No significant difference in complication rates was noted between former smokers and nonsmokers. Among smokers, patients with a smoking history of greater than 10 pack-years had a significantly higher overall complication rate compared with patients with a smoking history of 10 or fewer pack-years (55.8 percent versus 23.8 percent; p = 0.049). In summary, free TRAM flap breast reconstruction in smokers was not associated with a significant increase in the rates of vessel thrombosis, flap loss, or fat necrosis compared with rates in nonsmokers. However, smokers were at significantly higher risk for mastectomy skin flap necrosis, abdominal flap necrosis, and hernia compared with nonsmokers. Patients with a smoking history of greater than 10 pack-years were at especially high risk for perioperative complications, suggesting that this should be considered a relative contraindication for free TRAM flap breast reconstruction. Smoking-related complications were significantly reduced when the reconstruction was delayed or when the patient stopped smoking at least 4 weeks before surgery.     

Involuntary smoking and the risk of head and neck cancer in an East Asian population

BackgroundAlthough tobacco involuntary smoking is an established risk factor for lung cancer, the association with head and neck cancer (HNC) is not established. We aimed to investigate this potential association in an East Asian population.MethodsWe conducted a multicenter case-control study in East Asia including eight centers. We restricted our analysis to never tobacco smokers (303 cases and 459 controls) and to never tobacco smokers/never alcohol drinkers (243 cases and 403 controls).ResultsAmong never tobacco smokers, involuntary smoking was associated with a 1.47-fold increase in risk of HNC (95%CI = 1.02, 2.13) and a 1.8-fold increase in the risk of oral cavity cancer (95%CI = 1.14, 2.92). Among never tobacco smokers who were also never alcohol drinkers, increased risks were detected for more than 3 h per day of involuntary smoking exposure and for 15 or more years of exposure. A dose-response relation was suggested for frequency of exposure (p for trend = 0.014) and for years of exposure (p for trend = 0.010) for oral cavity cancer. We did not detect strong increases in the risk of the other HNC subsites.ConclusionsOur study supports the association between involuntary smoking and the risk of HNC. The association may be stronger for oral cavity cancer than for other HNC subsites.     

Morbidity and survival in neonates ventilated for the respiratory distress syndrome.

In a retrospective analysis the records of all (210) infants ventilated to treat the respiratory distress syndrome over three years were reviewed. A mortality of 19% was found. Intraventricular haemorrhage was associated than a significant increase in mortality in infants of less with 30 weeks'' gestation (p less than 0.001) and was the commonest cause of death. Pneumothoraces developed in one third of babies regardless of gestational age but were significantly associated with an increase in mortality only in infants of 27-29 weeks'' gestation. Patent ductus arteriosus was present in 31 infants and was commoner in babies of very low birth weight. The presence of a patent ductus arteriosus was not associated with decreased survival but was significantly related to an increased need for prolonged respiratory support (p less than 0.001). Thirty six infants developed chronic lung disease, three of whom died. Comparison with data from earlier studies indicated a steady improvement over the past decade in outcome for infants ventilated for the respiratory distress syndrome.