The effect of smoking on the outcome of in-vitro fertilization--embryo transfer

This study investigated the influence of cigarette smoking on the outcome of in-vitro fertilization-embryo transfer. Forty-one women under the age of 37 years, suffering from mechanical infertility, were suppressed with gonadotrophin releasing analogue from day 21 of the cycle. Twenty women were smokers and 21 women were non-smokers. Gonadotrophin releasing analogue was injected daily before ovarian stimulation with gonadotrophin was begun. The follicular phase was longer and the number of human menopausal gonadotrophin ampoules required to reach adequate stimulation were higher in smokers. The peak serum oestradiol level was not significantly different in smokers compared to non-smokers. However, follicular fluid levels of oestradiol were significantly lower in smokers than in non-smokers (657 +/- 367 versus 1077 +/- 786 ng/ml) respectively. Furthermore, the fertilization rate was also lower in smokers than in non-smokers (40.9 versus 61.7%) respectively. Four pregnancies were achieved in the non-smokers group, while only one ectopic pregnancy was diagnosed in the smokers group. These findings suggest that cigarette smoking has a detrimental effect on the outcome of in-vitro fertilization and embryo transfer.     

Risk factors for human herpesvirus 8 seropositivity in the AIDS Cancer Cohort Study.

BACKGROUND: Cigarette smoking has been associated with a decreased risk for AIDS-related and classical KS, but whether it is associated with decreased risk of human herpesvirus 8 (HHV-8) infection is unknown. STUDY DESIGN: We evaluated factors associated with HHV-8 seropositivity in 2795 participants (132 with KS) in the National Cancer Institute AIDS Cancer Cohort, including 1621 men who have sex with men (MSM), 660 heterosexual men and 514 women. Odds ratios (OR) and 95% confidence intervals were estimated using logistic regression models. RESULTS: Among non-KS subjects, HHV-8 seropositivity was 6%, 13% and 29% among women, heterosexual men and MSM, respectively. HHV-8 seropositivity was decreased in heavier (> or =1/2 pack/day) compared to lighter smokers among women (5% versus 8%; adjusted OR (aOR) 0.4; 95% CI 0.2-0.8) and MSM (27% versus 32%; aOR 0.7; 95% CI 0.6-1.0), but not among heterosexual men (12% versus 16%; aOR 0.7; 95% CI 0.4-1.2). HHV-8 seroprevalence was increased in heavier (> or =1 drink/day) compared to lighter consumers of alcohol among women (16% versus 4%; adjusted OR 5.2; 95% CI 2.3-12), but not among MSM (33% versus 28%; aOR 1.2; 95% CI 0.9-1.6) or heterosexual men (13% versus 13%; aOR 1.1; 95% CI 0.6-2.0). In analyses adjusted for smoking and drinking, HHV-8 seropositivity was positively associated with chlamydia infection (OR=4.3; 95% CI 1.2-13) and with marital status among women p(heterogeneity)=0.03, and with hepatitis (OR=1.6; 95% CI 1.2-2.1), gonorrhea (OR=1.5; 95% CI 1.1-1.9), genital warts (OR=1.5; 95% CI 1.1-2.0) and nitrate inhalant use (OR=1.7; 95% CI 1.3-2.3) among MSM. CONCLUSIONS: Inverse association of HHV-8 seropositivity with cigarette smoking may indicate protective effect of tobacco smoke on HHV-8 infection, whereas positive associations with alcohol may reflect either behavioral factors or biological effects modulating susceptibility. Smoking and drinking may influence KS risk, at least in part, by altering the natural history of HHV-8 infection.     

Maternal smoking in pregnancy and birth defects: a systematic review based on 173 687 malformed cases and 11.7 million controls

BACKGROUND ; There is uncertainty over whether maternal smoking is associated with birth defects. We conducted the first ever comprehensive systematic review to establish which specific malformations are associated with smoking. METHODS ; Observational studies published 1959-2010 were identified (Medline), and included if they reported the odds ratio (OR) for having a non-chromosomal birth defect among women who smoked during pregnancy compared with non-smokers. ORs adjusted for potential confounders were extracted (e.g. maternal age and alcohol), otherwise unadjusted estimates were used. One hundred and seventy-two articles were used in the meta-analyses: a total of 173 687 malformed cases and 11 674 332 unaffected controls. RESULTS ; Significant positive associations with maternal smoking were found for: cardiovascular/heart defects [OR 1.09, 95% confidence interval (CI) 1.02-1.17]; musculoskeletal defects (OR 1.16, 95% CI 1.05-1.27); limb reduction defects (OR 1.26, 95% CI 1.15-1.39); missing/extra digits (OR 1.18, 95% CI 0.99-1.41); clubfoot (OR 1.28, 95% CI 1.10-1.47); craniosynostosis (OR 1.33, 95% CI 1.03-1.73); facial defects (OR 1.19, 95% CI 1.06-1.35); eye defects (OR 1.25, 95% CI 1.11-1.40); orofacial clefts (OR 1.28, 95% CI 1.20-1.36); gastrointestinal defects (OR 1.27, 95% CI 1.18-1.36); gastroschisis (OR 1.50, 95% CI 1.28-1.76); anal atresia (OR 1.20, 95% CI 1.06-1.36); hernia (OR 1.40, 95% CI 1.23-1.59); and undescended testes (OR 1.13, 95% CI 1.02-1.25). There was a reduced risk for hypospadias (OR 0.90, 95% CI 0.85-0.95) and skin defects (OR 0.82, 0.75-0.89). For all defects combined the OR was 1.01 (0.96-1.07), due to including defects with a reduced risk and those with no association (including chromosomal defects). CONCLUSIONS ; Birth defects that are positively associated with maternal smoking should now be included in public health educational materials to encourage more women to quit before or during pregnancy.     

Risk Factors of Acoustic Neuroma: Systematic Review and Meta-Analysis

PurposeMany epidemiological studies have investigated environmental risk factors for the development of acoustic neuroma. However, these results are controversial. We conducted a meta-analysis of case-control studies to identify any potential relationship between history of noise exposure, smoking, allergic diseases, and risk of acoustic neuroma.ResultsEleven case-control studies were included in our meta-analysis. Acoustic neuroma was found to be associated with leisure noise exposure [odds ratio (OR)=1.33, 95% confidence interval (CI): 1.05–1.68], but not with occupational noise exposure and ever noise exposure (OR=1.20, 95% CI: 0.84–1.72 and OR=1.15, 95% CI: 0.80–1.65). The OR of acoustic neuroma for ever (versus never) smoking was 0.53 (95% CI: 0.30–0.94), while the subgroup analysis indicated ORs of 0.95 (95% CI: 0.81–1.10) and 0.49 (95% CI: 0.41–0.59) for ex-smoker and current smoker respectively. The ORs for asthma, eczema, and seasonal rhinitis were 0.98 (95% CI: 0.80–1.18), 0.91 (95% CI: 0.76–1.09), and 1.52 (95% CI: 0.90–2.54), respectively.ConclusionOur meta-analysis is suggestive of an elevated risk of acoustic neuroma among individuals who were ever exposed to leisure noise, but not to occupational noise. Our study also indicated a lower acoustic neuroma risk among ever and current cigarette smokers than never smokers, while there was no significant relationship for ex-smokers. No significant associations were found between acoustic neuroma and history of any allergic diseases, such as asthma, eczema, and seasonal rhinitis.     

Is sputum cytology reliable for detection of atypical lung epithelial proliferative changes triggered by cigarette smoking?

Background: In recent years, Saudi Arabia has witnessed major tobacco smoking-related disease, such as cardiovascular disease and cancer, particularly among the younger population. Methodology: The present study aimed at evaluating the effect of cigarette smoke on lung epithelial cells. Results: This was a cross-sectional case-control study involving 300 apparently healthy volunteers living in Ha’il, Northern Saudi Arabia. Cigarette smokers (N = 100) were used as cases, and non-smokers (N = 200) were used as controls. A sputum specimen was obtained from each participant, employing all necessary safety precautions and sample adequacy measures. Results: Among 300 study subjects, cytologic atypia was identified in 14/300 (4.7%). Among the 14 cases with atypical cytologic changes, 13/14 (92.9%) were in smokers and 1/14 (7.1%) was in a non-smoker. The risk of lung cytologic atypia associated with cigarette smoking, was OR (95% CI) = 29.73 (3.82-230.87), P = 0.0001. Out of 300 study subjects, metaplasia was identified in 45/300 (15%). Among 45 cases with metaplastic changes, 26/45 (57.8%) were in the smokers and 19/45 (42.2%) were in non-smokers. The risk of lung epithelial metaplasia associated with cigarette smoking was OR (95% CI) = 3.34 (1.74-6.41), P = 0.0003. Conclusion: Cigarette smoking is a significant risk for developing lung epithelial atypia, lung metaplasia, and inflammatory cell infiltrate (especially chronic inflammation). Sputum cytology is a simple, non-invasive method that can be used in screening at-risk populations for early detection of lung proliferative changes associated with tobacco smoking.     

Progress in searching for susceptibility loci and genes for smoking-related behaviour

Smoking behaviour is influenced by both genetic and environmental factors. Many years of twin and adoption studies have demonstrated that heritability is at least 50% responsible for both smoking initiation and smoking persistence. Furthermore, the extent, to which genetic and environmental factors contribute to smoking behaviour, is significantly different in men and women. Linkage analyses from several independent studies provide evidences for suggested linkage of smoking behaviour to chromosomes 1, 2, 4, 5, 6, 9, 10, 11, 14, 17, 18 and 21. However, almost none of these loci have been replicated yet. Furthermore, numerous population-based association studies have been performed to examine the effects of a number of candidate genes, such as cytochrome P450, dopamine receptor (DR) and transporter, serotonin transporter and nicotinic acetylcholine receptor, on smoking behaviour. However, many of these reports have not yet received independent confirmation. Of these candidate genes, the D2 dopamine receptor (DRD2) gene has been extensively studied. Meta-analysis of 12 reported studies showed a significantly higher prevalence of the DRD2 TaqI A1 allele in smokers than that in non-smokers (p < 0.0001; pooled OR = 1.50; 95% CI = 1.33-1.70). For other candidate genes, insufficient published studies are available to allow a meta-analysis to be performed, or meta-analysis showed no significant difference between smokers and non-smokers. More studies are necessary to determine whether these genes play a significant role in smoking behaviour.     

Glutathione S-transferase T1-null genotype interacts synergistically with heavy smoking on lung cancer risk

We studied the influence of genotype for glutathione S-transferase T1 (GSTT1) on susceptibility to lung cancer among 184 Swedish lung cancer patients (88 never-smokers and 96 ever-smokers) and 162 matched population controls (79 never-smokers and 83 ever-smokers), with special emphasis on gene-environment interactions. Cases had significantly lower frequency of the GSTT1-null genotype than that of controls among never-smokers (4.6 vs. 16.5%, P = 0.02), whereas the frequencies were very close to each other among smokers (7.4 vs. 7.2%). Cases with high packyears of smoking, however, had a significantly higher frequency of the GSTT1-null genotype compared to that of cases with low packyears (18.3 vs. 5.6%, P = 0.005). Adjusted for age and gender, the GSTT1-null genotype appeared to be protective against lung cancer among never-smokers (odds ratio [OR] = 0.2, 95% confidence interval [CI] = 0.07-0.7), although it was associated with an increased risk for lung cancer among smokers (OR = 2.1, 95% CI = 0.8-5.9), mainly attributed to the group of heavy smokers (>23 packyears; OR = 3.5, 95% CI = 0.7-17.3). Heavy smoking conferred a threefold increased risk for lung cancer (OR = 2.6, 95% CI = 1.3-5.0) among GSTT1-positive individuals, but a ninefold increased risk when combined with the GSTT1-null genotype (OR = 9.3, 95% CI = 1.9-46.3, relative to GSTT1-positive light smokers). This joint effect was further demonstrated by a positive interaction between the GSTT1-null genotype and packyears of smoking. The risk of lung cancer increased steeply with increasing packyears among GSTT1-null smokers, whereas no such effect was seen among GSTT1-positive smokers. We conclude that the GSTT1-null genotype may strengthen the effect of heavy smoking on lung cancer risk.     

Effects of cigarette smoking upon clinical outcomes of assisted reproduction: a meta-analysis

BACKGROUND: The aim of this meta-analysis was to investigate whether anydifference exists in success rate of clinical outcomes of assistedreproductive technologies (ART) between women who actively smokecigarettes at the time of treatment and those who do not. METHODS: An intensive computerized search was conducted on publishedliterature from eight databases, using search terms relatedto smoking, assisted reproduction and outcome measures. Eligiblestudies compared outcomes of ART between cigarette smoking patientsand a control group of non-smoking patients and reported onlive birth rate per cycle, clinical pregnancy rate per cycle,ectopic pregnancy rate per pregnancy or spontaneous miscarriagerate per pregnancy, and 21 studies were included in the meta-analyses.Pooled odds ratios (OR) and 95% confidence intervals (CI) werecalculated for the data, and statistical heterogeneity was testedfor using ² and I² values. A systematic review examined theeffect of smoking upon fertilization rates across 17 studies. RESULTS: Smoking patients demonstrated significantly lower odds of livebirth per cycle (OR 0.54, 95% CI 0.30–0.99), significantlylower odds of clinical pregnancy per cycle (OR 0.56, 95% CI0.43–0.73), significantly higher odds of spontaneous miscarriage(OR 2.65, 95% CI 1.33–5.30) and significantly higher oddsof ectopic pregnancy (OR 15.69, 95% CI 2.87–85.76). Asystematic literature review revealed that fertilization rateswere not significantly different between smoking and non-smokinggroups in most studies. CONCLUSIONS: This meta-analysis provides compelling evidence for a significantnegative effect of cigarette smoking upon clinical outcomesof ART and should be presented to infertility patients who smokecigarettes in order to optimize success rates.     

Limb deficiency defects, MSX1, and exposure to tobacco smoke

There is increasing evidence from epidemiologic studies that genetic susceptibilities may modify the teratogenic effects of smoking. A previous study suggested that maternal smoking in the presence of a dinucleotide repeat polymorphism for MSX1 produced an almost fivefold increased risk for limb anomalies, providing evidence for a gene-environment interaction. The current study examined this potential interaction, using case-control data with several methodologic improvements, including a larger sample size and more detailed information on cigarette smoke exposures. Cases (n = 92) were ascertained from pregnancies ending in 1987-1989, and controls (n = 180) were randomly selected from eligible liveborn infants. In telephone interviews, women reported smoking behaviors during the month before pregnancy through the end of the first trimester. Odds ratios (OR) for maternal and paternal smoking ranged from 1.0 to 1.4, risk estimates were imprecise; for example, the OR for maternal smoking >or=20 cigarettes per day, versus none, was 1.3 (95% confidence interval (CI) 0.5-3.4). Relative to the homozygous wildtype, the OR was 1.5 (95% CI 0.7-3.5) for the homozygous variant genotype and 0.8 (95% CI 0.5-1.4) for the heterozygous variant genotype. There was no evidence that maternal smoking or both parents smoking, in combination with a susceptible MSX1 genotype, conferred an additional increase in risk of limb defects. This study did not find a gene-environment interaction between maternal smoking, infant MSX1 CA repeat polymorphism, and risk of limb deficiency defects. This finding contrasts with results of a previous study, which provided initial evidence for such an interaction. Several important methodological differences may have contributed to the differences in findings between the two studies.     

Smoking behaviour as a predictor of depression among Finnish men and women: a prospective cohort study of adult twins

BACKGROUND: Depression is associated with smoking, but the causality of the relationship is debated. The authors examine smoking behaviour as a predictor of depression among the Finnish adult twin population. METHOD: Based on responses to surveys in 1975 and 1981, the authors characterized the subjects as never smokers, persistent former smokers, quitters, recurrent smokers and persistent smokers. The Beck Depression Inventory (BDI) was applied in 1990 to measure depression (BDI score >9). Although the population consisted of twins, the authors first considered the subjects as individuals. Logistic regression models were computed for 4164 men and 4934 women. In order to control for family and genetic background, conditional logistic regression analyses were conducted among twin pairs discordant for depression. Bivariate genetic modelling was used to examine genetic and environmental components of the correlation between smoking and depression. RESULTS: Among the men, persistent smoking (OR 1 x 42, 95% CI 1 x 07-1 x 89) and smoking in 1975 but quitting by 1981 (OR 1 x 68, 95% CI 1 x 17-2 x 42) was associated with a higher risk of depression, while among the women only the quitters had an elevated risk (OR 1 x 38, 96% CI 1 x 01-1 x 87). The gender x smoking interaction showed persistent smoking to be a stronger risk for men. When family and genetic background were controlled, smoking remained a predictor of depression. Genetic modelling among the men suggested a modest correlation (rg=0 x 25) between genetic components of smoking and depression. CONCLUSIONS: Smoking behaviour may be a gender-sensitive predictor of depression, the stronger association in men being partly accounted for by having underlying genes in common.     

Mid-life smoking and late-life dementia: the Honolulu-Asia Aging Study

We studied the association between mid-life smoking and late-life dementia in the Honolulu Heart Program (1965-1971) and follow-up assessment for dementia (1991-1996) of 3734 Japanese-American men (80% of survivors). Neuropathologic data were available for 218 men. Adjusting for age, education and apolipoprotein E (APOE) genotype, the risk of Alzheimer's disease (AD) in smokers increased with pack-years of smoking at medium (odds ratio (OR)=2.18, 95% confidence interval (CI)=1.07-4.69) and heavy (OR=2.40; 95% CI=1.16-5.17) smoking levels. Very heavy smoking was not associated with AD (OR=1.08; 95% CI=0.43-2.63). Findings were similar when AD cases included those with cerebrovascular disease and for all dementias combined. Adjustment for cardiovascular and respiratory factors or stratification by apolipoprotein E genotype did not change these associations. In an autopsied subsample, the number of neuritic plaques increased with amount smoked. This study suggests that amount smoked is associated with an increasing risk of AD and Alzheimer-type neuropathology up to heavy smoking levels. The lack of association in very heavy smokers may be due to a hardy survivor effect.     

Cigarette smoking and Parkinson's disease: a meta-analysis

Many but not all studies have indicated that smoking is inversely associated with Parkinson's disease (PD). Meta-analysis of epidemiological studies on smoking and PD was performed to summarize data from published studies. Fifty-four epidemiological studies (48 case-control and 6 cohort studies, 53 publications) were identified for potential inclusion in meta-analysis. The summary risk estimates for current smokers, former smokers, and ever (current and former) smokers were 0.31 (95% confidence interval (CI) = 0.25-0.38), 0.72 (95% CI = 0.63-0.83) and 0.55 (95% CI = 0.51-0.59), respectively. In stratified analysis by study design, smoking had a somewhat greater impact on PD risk in cohort studies than in case-control studies. However, meta-regression indicated that the study design did not significantly contribute to heterogeneity. Additional analyses were restricted to case-control studies because of the sufficient number of studies. Stratified analysis by ethnicity indicated that the summary OR for ever-smokers was nonsignificantly smaller in Asian populations than in Caucasian populations. In stratified analysis by source of controls, former smoking was significantly associated with a decreased risk of PD in hospital-based case-control studies but was marginally associated with a decreased risk in population-based case-control studies. The source of controls did not contribute significantly to heterogeneity. PD risk associated with ever-smoking was significantly lower for a hospital-based approach than a population-based approach. Among current smokers, the association held true to the same extent for both approaches. This meta-analysis indicated that smokers have a lower risk of PD. As PD is a multifactorial disease, further investigation of the smoking-gene interaction on PD risk may lead to a better understanding of the pathogenesis of PD.     

Inhaled medication usage in post-menopausal women and lifetime tobacco smoke exposure: The Women’s Health Initiative Observational Study

ObjectiveWhile active smoking is a causal agent in respiratory disease, the independent role of secondhand smoke (SHS) merits further investigation. We investigated associations between lifetime active smoking and exposure to secondhand smoke – studied independently – and current use of 1 or more inhaled medications as a surrogate for prevalent pulmonary disease in post-menopausal women.Study designInformation on lifetime active and passive tobacco exposure and inhaled pulmonary medication usage at enrollment was collected from 88,185 postmenopausal women aged 50–79 enrolled in the Women’s Health Initiative Observational Study from 1993 to 1998 at 40 centers in the United States. Participants were recruited from localities surrounding the study centers using a variety of methods, including informational mailings and mass media campaigns.Main outcome measuresMultivariate adjusted regression models were used to estimate odds ratios and 95% CI according to levels of active smoking and SHS exposure, and trends were tested across categories.ResultsEver active smokers had an overall OR of 1.97 (95% CI 1.58–2.45) for having one or more prescribed inhaled medication compared with never-smoking women not exposed to active or passive smoke. The overall OR for using inhalers for never-smoking women exposed to any SHS compared with the same reference group was 1.33 (95% CI 1.07–1.65). In a quantified analysis of SHS, never-smoking women with the highest levels of lifetime SHS exposure had an estimated risk of inhaled medication usage of 1.74 (95% CI 1.32–2.30).ConclusionsThe risk of requiring one or more prescribed inhaled medications for pulmonary disease was significantly higher in post-menopausal women who ever smoked or who had lifetime exposure to SHS.     

The impact of cigarette smoking on human semen parameters and hormones

BACKGROUND: In this prospective study, semen parameters and hormone concentrations of infertile smokers were compared with infertile non- and ex-smokers. We also determined how many men with idiopathic infertility would stop smoking in an attempt to improve their fertility. METHODS: 1104 men (517 non-smokers, 109 ex-smokers and 478 smokers) with infertility for at least 1 year were evaluated. Evaluation included medical history, physical examination, hormone analysis and two semen analyses. Prior to the second semen analysis, smokers were urged to quit smoking. RESULTS: Smokers were significantly younger (P < 0.001), had significantly more round cells in their ejaculates (P = 0.003), and the percentage of ejaculates with > 1 x 10(6)/ml leukocytes was higher in smokers (P < 0.001). Increased free and total serum testosterone (P < 0.001) and decreased prolactin levels (P < 0.001) were found in smokers. No differences were found between non-smokers and ex-smokers. Only 23.1% of the smokers versus 46% non-smokers (P < 0.001) returned for a second semen analysis, 14 of whom reduced and 15 of whom quit smoking completely. Testosterone levels were significantly lower in those who were able to stop or reduce smoking (P < 0.001). CONCLUSIONS: Smoking does not affect conventional semen parameters, but significantly increases round cells and leukocytes. Only a few idiopathic infertile smokers were able to quit smoking.     

Pregnancy: Coffee and alcohol intake, smoking and risk of multiple pregnancy

We analysed the relationship between coffee and alcohol intake,smoking and risk of multiple pregnancies using data from a case-controlstudy on risk factors for multiple births conducted in Italy.Cases were 133 women who delivered multiple births not relatedto treatment for infertility (33 monozygotic and 100 dizygotictwins). Controls were 395 women admitted for normal deliveryat the same clinic where cases had been identified. The oddsratios (OR) of multiple pregnancy were 1.5 [95% confidence interval(CI) 0.8–2.8] and 2.0 (95% CI 1.0–3.7) for womendrinking respectively one to two or three or more cups of coffeeper day in comparison with non-coffee drinkers. Consideringseparately dizygotic and monozygotic pregnancies, the estimatedOR were respectively for women drinking three or more cups ofcoffee, 1.7 and 3.1 for dizygotic and monozygotic pregnancies.The risk of multiple pregnancy tended to be higher in womendrinking 15 alcohol drinks per week: in comparison with tea-totallersthe estimated OR for drink 15 glasses per week were 23 and 2.6respectively for dizygotic and monozygotic pregnancies. Heavysmokers (10 cigarettes per day) were at increased risk of multiplepregnancy: in comparison with never smokers, the estimated ORfor multiple pregnancy was 1.6 (95% CI 0.9–2.7). Consideringseparately the two groups of multiple pregnancy, the OR of dizygoticand monozygotic pregnancy were 1.4 (95% CI 0.8–2.5) and2.4 (95% CI 0.9–6.1) for women smoking 10 cigarettes/day, but the trend in risk with number of cigarettes smokedper day and duration of the habit was not significant.     

Cigarette smoking and outcomes of in-vitro fertilization and embryo transfer: a prospective cohort study.

A prospective cohort study of 222 consecutive couples undergoing 297 cycles of in-vitro fertilization and embryo transfer (IVF-ET) was conducted to evaluate the impact of cigarette smoking in males and females. Compared with non-smokers, females smoking at the time of treatment had more previous pregnancies (1.16 versus 0.63, P less than 0.001), consumed more coffee per day (3.29 versus 1.85 cups, P = 0.001) and were less likely to hold a professional or skilled job (41% versus 66%). There was no difference in the response to ovarian stimulation in terms of the duration and dose of human menopausal gonadotrophin, peak oestradiol level or number of oocytes retrieved. The fertilization rate was actually higher in heavy smokers than in non-smokers (79.3% versus 61.3%, P = 0.007). The rate of embryo cleavage was retarded in a dose-dependent fashion. In smokers of 1-14 cigarettes/day, the likelihood of transferring an embryo at greater than or equal to 4-cell stage was 0.87 [95% confidence limits (CL) 0.56-1.4] and in smokers of greater than or equal to 15 cigarettes/day, the likelihood was 0.52 (95% CL 0.31-0.88). However, evaluation of interrelated factors using logistic regression suggested that a low socioeconomic status had a greater detrimental effect on embryo cleavage rate than female smoking. No significant difference was noted in the clinical outcome following embryo transfer. A study of larger sample size is required to evaluate whether the effects of cigarette smoking are independent of socioeconomic status and other related factors and whether they result in reduced ongoing clinical pregnancy and live birth rates.     

The effect of reproductive history on future pregnancy outcomes.

The aim of this study was to examine the separate and joint effects of previous pregnancy history, year of pregnancy outcome, maternal age, height, smoking and fertility on risk of fetal death. Data were available from a study of female radiographers. Analyses were carried out on 3053 women with a total of 6993 pregnancies. Women reporting problems with conception or previous fetal losses had an increased risk of a pregnancy ending in a fetal death. In particular, women with primary or secondary infertility had an approximately fourfold increase in risk compared with women who reported no difficulties [odds ratio (OR): 3.92; 95% confidence interval (CI): (3.02, 5.07)]. This relationship was independent of pregnancy order and pregnancy history and was more marked in older maternal ages. The effect of pregnancy history was cumulative and possibly multiplicative in effect, with a threefold increase in the risk of losing a third pregnancy following two previous losses [OR: 3.19; 95% CI: (1.60, 6.35)]. There were no consistent patterns of risk associated with year of pregnancy outcome, maternal age, height or smoking status. These results suggest that previous pregnancy outcomes and problems with conception may be the strongest determinants of fetal loss in subsequent pregnancies.     

Smoking in young women in Scotland and future burden of hospital admission and death: a nested cohort study

Background

Many women smoke, yet few longitudinal studies have examined the non-fatal burden of smoking in women.

Aim

To investigate smoking in young women, and hospital admission and death in Scotland; and to compare mortality risk with elsewhere in the UK.

Design and setting

Nested cohort study: Royal College of General Practitioners’ Oral Contraception Study, UK.

Method

A total of 4121 women categorised by smoking habits and living in Scotland at recruitment (1968–1969) were followed until March 2009. Cox regression was used to investigate smoking and survival time; mortality from cancer, circulatory, or respiratory disease, and all other causes; and hospitalisation for any reason, and for specific reasons. The number and type of hospital admissions and bed-days were examined by smoking status. Life tables and Cox regression were used to compare the mortality risk of women living in Scotland with that of women living elsewhere.

Results

All-cause mortality was increased in women who smoked <15 cigarettes daily (adjusted hazard ratio = 1.99, 95% confidence interval [CI] = 1.74 to 2.27) and those who smoked ≥15 cigarettes daily (adjusted HR = 2.81, 95% CI = 2.47 to 3.20). Smoking any amount increased death from cancer, circulatory, respiratory, and other causes. Increased risk estimates were seen in one or both smoking groups for hospitalisation for any cause, and for several specific causes. More smokers than non-smokers were admitted to hospital, for four or more reasons, and had a longer total stay. The median survival age among smokers was lower in Scotland than elsewhere. Higher adjusted hazard ratios for mortality were found among smokers in Scotland.

Conclusion

This study provides a powerful reminder of the burden of smoking in young women. In the UK, harmful effects appear to be worse in smokers in Scotland.     

Acculturation and cigarette smoking among Korean American men

This study examined the prevalence and correlated factors of cigarette smoking in a cross-sectional, epidemiological survey of Korean American men living in Maryland (n=333). In this sample, 26.1% were current smokers and 42.3% were former smokers. The older age group (> or = 40 years) was more likely to have quit smoking than the younger age group (< 40 years). In multiple logistic regression analysis, acculturation was associated with smoking status; those who stayed more than 20 years in the U.S. were less likely to be current smokers (OR=0.32, 95% CI 0.13-0.77) than those who stayed less than 10 years. Alcohol use was associated with smoking status; those who consumed alcohol were more likely to be current smokers (OR=5.24, 95% CI 2.33-11.79) or former smokers (OR=5.45, 95% CI=2.69-11.04) than those did not. Those with hypertension were more likely to have quit smoking (OR=3.11, 95% CI=1.33-7.24). The results suggest that the role of acculturation in smoking status among Korean American men deserves further attention by researchers as well as by health professionals who develop smoking prevention and cessation programs.