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1.
BACKGROUND: The purpose of this study was to examine prospectively the relation of shift work to risk of coronary heart disease (CHD) in a cohort of women. METHODS AND RESULTS: An ongoing prospective cohort of US female nurses, in whom we assessed (in 1988) the total number of years during which they worked rotating night shifts (at least three nights per month in addition to day and evening shifts), included 79,109 women, 42 to 67 years old in 1988, who were free of diagnosed CHD and stroke. Incident CHD was defined as nonfatal myocardial infarction and fatal CHD. During 4 years of follow-up (1988 to 1992), 292 cases of incident CHD (248 nonfatal myocardial infarction and 44 fatal CHD) occurred. The age-adjusted relative risk of CHD was 1.38 (95% CI, 1.08 to 1.76) in women who reported ever doing shift work compared with those who had never done so. The excess risk persisted after adjustment for cigarette smoking and a variety of other cardiovascular risk factors. Compared with women who had never done shift work, the multivariate adjusted relative risks of CHD were 1.21 (95% CI, 0.92 to 1.59) among women reporting less than 6 years and 1.51 (95% CI, 1.12 to 2.03) among those reporting 6 or more years of rotating night shifts. CONCLUSIONS: These data are compatible with the possibility that 6 or more years of shift work may increase the risk of CHD in women.  相似文献   

2.
OBJECTIVES: This study tested the hypothesis that women who deliver small-for-gestational-age infants are more often exposed to passive smoking at home or at work. METHODS: Among a 1-year cohort of nulliparous women in the city of Malm?, Sweden 872 (87.7%) women completed a questionnaire during their first prenatal visit. The study was carried out among women whose pregnancies resulted in a singleton live birth (n = 826), 6.7% of infants were classified as small for their gestational age. RESULTS: Passive smoking in early pregnancy was shown to double a woman's risk of delivering a small-for-gestational-age infant, independent of potential confounding factors such as age, height, weight, nationality, educational level, and the mother's own active smoking (odds ratio [OR] = 2.7). A stratified analysis indicated interactional effects of maternal smoking and passive smoking on relative small-for-gestational-age risk. CONCLUSIONS: Based on an attributable risk estimate, a considerable reduction in the incidence of small-for-gestational-age births could be reached if pregnant women were not exposed to passive smoking.  相似文献   

3.
Nonmalignant respiratory disease (NMRD) mortality was examined among woodworkers participating in the American Cancer Society's CPS-II cohort study. During the 6-year prospective follow-up there were 97 NMRD death's among 11,541 men reporting employment in wood-related occupations and 1,338 NMRD deaths among 317,424 men reporting no exposure to wood dust or wood-related jobs. Relative risks, adjusted for age and smoking, were calculated using Poisson regression. A small excess of NMRD was observed among woodworkers. However, the relative risk was higher among woodworkers who did not report exposure to wood dust (RR = 1.52, 95% CI = 1.18-1.97) than those who did (RR = 1.27, 95% CI = 0.91-1.77), and no clear trend with duration of exposure was observed. An excess of NMRD was observed among woodworkers reporting exposure to asbestos (RR = 1.59, 95% CI = 0.85-2.96), as well as the small number of woodworkers reporting exposure to formaldehyde (RR = 1.95, 95% CI = 0.63-6.06), but men not reporting exposure to these substances also had an excess risk. Although limited by a short follow-up period and crude indicators of exposure, the strengths of this analysis were the ability to compare woodworkers to a similar, healthy population and to adjust for the effects of smoking. Cohort studies with better exposure information are needed to examine the role of occupational exposures among woodworkers in the etiology of respiratory disease.  相似文献   

4.
BACKGROUND: Results of several recent studies suggest that depression is predictive of incident coronary disease. However, few studies have examined this relationship in the elderly, the age at which most coronary heart disease (CHD) becomes clinically manifest. METHODS AND RESULTS: Data are from the New Haven, Conn, cohort (N = 2812) of the Established Populations for the Epidemiologic Studies of the Elderly project. Baseline information on depressive symptoms and CHD risk factors was collected during an in-person interview in 1982. Nonfatal myocardial infarctions were identified through monitoring of admissions to local hospitals and were validated by medical chart review. Cause of death was obtained from death certificates for all deceased participants. Outcomes were defined as CHD deaths (n = 255) and total incident CHD events (n = 391) between January 1, 1982, and December 31, 1991. There was no association between depressive symptoms and CHD outcomes in men. Among women, depressive symptoms were associated with an age-adjusted relative risk of 1.03 (per unit increase on the symptom scale) for CHD mortality (P=.001) and total CHD incidence (P=.002). These associations were largely unaffected by adjustment for established CHD risk factors but were reduced to nonsignificant levels after additional adjustment for impaired physical function. Additional analysis showed a significant association for depressive symptoms among women who had no physical function impairments or who survived at least 3 years without an event. CONCLUSION: Depressive symptoms may not be independent risk factors for CHD outcomes in elderly populations in general but may increase risk among relatively healthy older women.  相似文献   

5.
OBJECTIVE: Investigate risk factors for colon polyp using multivariate analyses. DESIGN: In a group responding to a 1992 mail survey, we assessed the association between physician-diagnosed colon polyp and possible risk factors reported primarily 10 years earlier. SETTING: Survey respondents within the Cancer Prevention Study II. PARTICIPANTS: Respondents, 72,868 men and 81,356 women, who reported no polyp diagnosis when questioned in 1982 at ages 40 to 64 years. MEASUREMENTS AND MAIN RESULTS: The characteristics of 7,504 men (10.3%) and 5,111 women (6.3%) reporting a first colon polyp were compared with those of participants who did not report a polyp. After adjustments for age, family history of colorectal cancer, and other potential risk factors, polyp occurrence was associated with 1982 histories of smoking, former smoking, alcohol use of at least two drinks per day (odds ratios [ORs] from 1.5 to 1.1; all p < .005), and a body mass index > or = 28 kg/m2 (men's OR 1.06; 95% confidence interval [CI] 1.00, 1.13; women's OR 1.08; 95% CI 0.99, 1.17). Polyps were also associated with a diagnosis of gallbladder disease or gallstone at any time and with gallbladder surgery up to 1982 (OR from 2.7 to 1.3; all p < .001). Polyp occurrence was inversely associated with 1982 histories of high exercise level (men's OR 0.83; 95% CI 0.76, 0.91; women's OR 0.90; 95% CI 0.78, 1.03), frequent aspirin use in women (OR 0.85; 95% CI 0.77, 0.95), and high parity in women (OR 0.84; 95% CI 0.75, 0.94). Among participants lacking a clinically normal gallbladder, the polyp risks associated with smoking and high body mass index were reduced (p < .04 for interactions). CONCLUSIONS: Despite the limitations and potential biases in these self-reported data, the risk factors described here may be useful for identifying persons at modestly increased risk of having a colon polyp. The effect-modifying role of gallbladder status deserves further investigation.  相似文献   

6.
To examine the effect of passive smoking on plasma fibrinogen, a coronary risk factor, a cross-sectional study was conducted between 1990 and 1993 for 1,780 Japanese women aged 45-74 years who resided in Kyowa town, Ibaraki-ken, Japan. Fibrinogen concentrations controlling for age, body mass index, ethanol intake, serum total cholesterol, diabetes mellitus, and menopausal status were 8.6 (95% confidence interval 1.6-15.6) mg/dl higher in women exposed passively to smoking outside the home (n = 435) and 11.2 (95% confidence interval 3.0-19.3) mg/dl higher in women exposed both in and outside the home (n = 272) than in women unexposed in either location (n = 524). These effects of passive smoking were about 40-60% of that of current active smoking. An effect of passive smoking at home only was small and not statistically significant. The association between fibrinogen and passive smoking was primarily observed in women aged 45-59 years but not in those aged 60-74 years. Passive smoking may raise the risk of coronary heart disease partly by increasing plasma fibrinogen concentrations.  相似文献   

7.
To examine the effects of smoking and N-acetylation genetics on breast cancer risk, we analyzed data from an ongoing, population-based, case-control study of invasive breast cancer in North Carolina. The study population consisted of 498 cases and 473 controls, with approximately equal numbers of African-American and white women, and women under the age of 50 and age 50 years or older. Among premenopausal women, there was no association between current smoking [odds ratio (OR), 0.9; 95% confidence interval (CI), 0.5-1.5] or past smoking (OR, 1.0; 95% CI, 0.6-1.6) and breast cancer risk. Among postmenopausal women, there was also no association with current smoking (OR, 1.2; 95% CI, 0.7-2.0); however, a small increase in risk was observed for past smoking (OR, 1.5; 95% CI, 1.0-2.4). For postmenopausal women who smoked in the past, ORs and 95% CIs were 3.4 (1.4-8.1) for smoking within the past 3 years, 3.0 (1.3-6.7) for smoking 4-9 years ago, and 0.6 (0.3-1.4) for smoking 10-19 years ago. Neither N-acetyltransferase 1 (NAT1) nor N-acetyltransferase 2 (NAT2) genotype alone was associated with increased breast cancer risk. There was little evidence for modification of smoking effects according to genotype, except among postmenopausal women. Among postmenopausal women, ORs for smoking within the past 3 years were greater for women with the NAT1*10 genotype (OR, 9.0; 95% CI, 1.9-41.8) than NAT1-non*10 (OR, 2.5; 95% CI, 0.9-7.2) and greater for NAT2-rapid genotype (OR, 7.4; 95% CI, 1.6-32.6) than NAT2-slow (OR, 2.8; 95% CI, 0.4-8.0). Future studies of NAT genotypes and breast cancer should investigate the effects of environmental tobacco smoke, diet, and other exposures.  相似文献   

8.
BACKGROUND: Cigarette smoking has been shown to increase oxidative DNA damage in human sperm cells. Assessment of the role of cigarette smoking in the etiology of childhood cancer has focused primarily on the effect of maternal smoking. Similar studies in relation to paternal smoking, however, have been inconclusive. Few studies have evaluated the effect of paternal smoking in the preconception period, and most of these could not disentangle the effects of paternal from maternal smoking. PURPOSE: We investigated the relationship of paternal smoking, particularly in the preconception period, with childhood cancer among offspring of the nonsmoking mothers. METHODS: We conducted a population-based, case-control study in Shanghai, People's Republic of China, where the prevalence of smoking is high among men but extremely low among women. The study included 642 childhood cancer case patients (<15 years of age) and their individually matched control subjects. Information concerning parental smoking, alcohol drinking, and other exposures of the index child was obtained by direct interview of both parents of the study subjects. Odds ratios (ORs), derived from conditional logistic regression models, were used to measure the association between paternal smoking and risk of childhood cancers. RESULTS AND CONCLUSIONS: Paternal preconception smoking was related to a significantly elevated risk of childhood cancers, particularly acute leukemia and lymphoma. The risks rose with increasing pack-years of paternal preconception smoking for acute lymphocytic leukemia (ALL) (P for trend = .01), lymphoma (P for trend = .07), and total cancer (P for trend = .006). Compared with children whose fathers had never smoked cigarettes, children whose fathers smoked more than five pack-years prior to their conception had adjusted ORs of 3.8 (95% confidence interval [CI] = 1.3-12.3) for ALL, 4.5 (95% CI = 1.2-16.8) for lymphoma, 2.7 (95% CI = 0.8-9.9) for brain tumors, and 1.7 (95% CI = 1.2-2.5) for all cancers combined. Statistically significant increased risks of cancer were restricted to children under the age of 5 years at diagnosis or those whose fathers had smoked during all of the 5 years prior to conception. IMPLICATIONS: Further studies are needed to confirm the association of paternal smoking with increased risk of cancer in offspring, to clarify the pattern of risks in relation to the timing of cigarette smoking, and to elucidate the biologic mechanism involved in predisposing the offspring to cancer. For example, it may be that paternal smoking induces prezygotic genetic damage that, in turn, acts as the predisposing factor.  相似文献   

9.
Narghile smoking, a common habit among women in many non-Western societies, is assumed by the public to be minimally harmful. This study aims at identifying the effect of smoking narghiles during pregnancy on the weight of the newborn and other pregnancy outcomes. Three groups of pregnant women were interviewed in several hospitals in Lebanon between 1993 and 1995: 106 who smoked narghiles during their pregnancy, 277 who smoked cigarettes, and 512 who did not smoke. The adjusted mean birth weight of babies born to women who smoked one or more narghiles a day during pregnancy and to women who started smoking in the first trimester was more than 100 g less than that of babies born to nonsmokers (p < 0.1). The adjusted odds ratio of having babies with low birth weight (<2,500 g) among the narghile smokers was 1.89 (95% confidence interval (CI) 0.67-5.38). The risk increased to 2.62 (95% CI 0.90-7.66) among those who started smoking narghiles in the first trimester. A stronger association and a dose-response relation were found among cigarette smokers. The association between narghile smoking and other pregnancy outcomes, especially Apgar score and respiratory distress, was also noticeable. Further research and a policy action to fight the misperception that narghile smoking is safe are both recommended.  相似文献   

10.
BACKGROUND: The relation of parental smoking to wheezing and asthma occurring after the first year of life was assessed by a systematic quantitative review of case-control and longitudinal studies, complementing earlier reviews of cross sectional surveys and wheezing in early childhood. METHODS: Fifty one relevant publications were identified after consideration of 1593 abstracts selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search was completed in April 1997 and identified six studies of asthma incidence, seven of prognosis, 22 case-control studies, and 10 case series addressing disease severity. RESULTS: Maternal smoking was associated with an increased incidence of wheezing illness up to age 6 (pooled odds ratio 1.31, 95% CI 1.22 to 1.41), but less strongly thereafter (1.13, 95% CI 1.04 to 1.22). The long term prognosis of early wheezing illness was better if the mother smoked. The pooled odds ratio for asthma prevalence from 14 case-control studies was 1.37 (95% CI 1.15 to 1.64) if either parent smoked. Four studies suggest that parental smoking is more strongly associated with wheezing among non-atopic children. Indicators of disease severity including symptom scores, attack frequency, medication use, hospital attendance, and life threatening bronchospasm were in general positively related to household smoke exposure. CONCLUSIONS: The excess incidence of wheezing in smoking households appears to be largely non-atopic "wheezy bronchitis" with a relatively benign prognosis, but among children with established asthma, parental smoking is associated with more severe disease. This apparent paradox may be reconciled if environmental tobacco smoke is considered a co-factor provoking wheezing attacks, rather than a cause of the underlying asthmatic tendency.  相似文献   

11.
Objective: No studies have examined the relationship between caregiver beliefs about the risks of smoking to their own health and caregiver beliefs about the effect of their smoking on their child's health. In the current study, we investigated our proposed risk congruence hypothesis among caregivers who smoke. Specifically, we investigated whether caregivers' self-perceived risk of smoking is directly associated with their perception of the risks of smoking to their child. Method: The sample consisted of 271 regular smokers (≥3 cigarettes per day; Mage = 32.9 years; 214 women) who were caregivers of children with asthma (Mage = 4.9 years) who had a recent visit to the emergency room for their asthma. Three constructs of perceived risk were measured via self-report questionnaires assessing both caregiver perception of smoking risk to self and to child: Precaution Effectiveness, Optimistic Bias, and Perceived Vulnerability. Child asthma-related functional morbidity and home and child secondhand smoke exposure were also assessed. Results: Consistent with our risk congruence hypothesis, self-perceived risk of smoking was significantly associated with perceived risk to child, over and above the child's secondhand smoke exposure and caregiver report of child's asthma symptoms (i.e., asthma-related functional morbidity). Conclusions: These findings should be considered in the design of clinical interventions seeking to influence risk of caregiver behavior on child health. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

12.
In a cohort study of 1080 pupils who were followed for 5 years from when they left compulsory school (from age 16 to age 21 years), smoking habits were found to correlate with unemployment among both boys and girls. Pupils who were smokers in school had a higher risk of becoming unemployed than non-smokers. Irrespective of early smoking, smoking habits developed more unfavourably among unemployed young people than among those with no unemployment during the period studied. The odds ratio of being a smoker at the age of 21 years when unemployed more than 20 weeks during the observation period, compared with those without or with short unemployment, was 2.44 for men and 3.45 for women. When adjusted for the influence of socio-economic background, education, economy and smoking habits at the start of the period, the odds ratio was 1.7 (95% CI 1.01-2.86) for men and 2.0 (1.13-3.53) for women. The adjusted odds ratio for increasing or starting smoking during the period was 1.5 (95% CI 0.89-2.56) for men and 2.0 (1.18-3.35) for women. No significant correlation was found between snuffing and unemployment. Thus, it seems that unemployment is a risk factor for development of tobacco smoking in young people, especially among women.  相似文献   

13.
OBJECTIVE: To investigate possible associations between tobacco smoking and alcohol consumption and the risk of adult glioma. DESIGN: This was a population based, case-control study. Relative risks (RR) were estimated using logistic regression analysis. SETTING: Melbourne, Australia. PARTICIPANTS: These comprised 416 case subjects (166 women, 250 men), 66% of those eligible; and 422 control subjects (170 women, 252 men), 43.5% of those potentially eligible. RESULTS: There was no increase in risk of glioma with having ever smoked tobacco (RR 1.29, 95% CI 0.95, 1.75) for all subjects, adjusted for age, a reference date, and gender. There was a slight increase in risk for men (RR 1.64, 95% CI 1.1, 2.45), but not for women (RR 0.99, 95% CI 0.62, 1.62). For men, there was no increase in risk with increasing pack-years of cigarette smoking, but the risk was significantly increased in subjects who had smoked for less than 10 years. There was no increase in risk associated with having ever drunk alcohol for all subjects (RR 0.96, 95% CI 0.67, 1.37), women (RR 0.69, 95% CI 0.4, 1.15) or men (RR 1.40, 95% CI 0.81, 2.43). CONCLUSIONS: This study does not support an association between either tobacco smoking or alcohol consumption and glioma. The pattern of risk associated with tobacco smoking in men appears inconsistent with a causal role, and may be due to chance, response bias, or uncontrolled confounding.  相似文献   

14.
Animal experiments suggest that the fetal brain is sensitive to nicotine. Although much attention has been given to the relation between cigarette smoking during pregnancy and neurodevelopment in children, this remains controversial. Our study describes the relationship between maternal cigarette smoking during pregnancy and babbling abilities of the 8-month-old infant. In a longitudinal cohort, information was collected at the 16th week of gestation, at delivery and when the infant was about 8 months old. At this age babbling abilities of the infant were evaluated by a health visitor during a home visit. Singleton infants without any disability born at Aarhus University Hospital, Denmark, 1991-92 and still living in the Community of Aarhus at the age of 8 months were eligible (n = 2302). Complete follow-up was obtained for 1871 children (81.3%). A dose-response-like relationship between number of cigarettes smoked per day during pregnancy and babbling abilities was found after controlling for potential confounders. Smoking 10 or more cigarettes per day during pregnancy almost doubled the risk (odds ratio [OR] = 2.0, 95% confidence interval [CI] 1.1-3.6) of the infant being a non-babbler at the examination at 8 months. Among children who were breast fed for less than 4 months this risk was even higher (OR = 2.7, CI 1.3-5.8).  相似文献   

15.
The association between maternal smoking during pregnancy and childhood cancer was investigated using prospectively collected data from 54,795 liveborn children in the Collaborative Perinatal Project (1959-1966). Cases of cancer had a histologic diagnosis and/or a compatible clinical course. There were 51 children with cancer, for a cumulative incidence of cancer of 1.1 per 1,000 by 96 months of age. Maternal smoking was determined at each prenatal visit; 52% of mothers reported smoking at one or more visits. By age 8 years, cancer had occurred in 1.4 per 1,000 children whose mothers did not smoke during pregnancy, compared with 0.9 per 1,000 children whose mothers smoked (p = 0.15 by log rank test); the hazard ratio was 0.67 (95% confidence interval (CI) 0.38-1.17). There was no dose-response effect of smoking compared with nonsmokers (hazard ratio for one to 10 cigarettes/day = 0.45, more than 10 cigarettes/day = 0.83). The hazard ratio for leukemia among children whose mothers smoked was 0.82 (95% CI 0.31-2.11); the hazard ratio for cancers other than leukemia was 0.60 (95% CI 0.30-1.20). Adjustment did not change the hazard ratio substantially. Although the relatively small number of cases precluded extensive study of individual types of cancer, the authors conclude that maternal smoking during pregnancy is not associated with an increased risk of childhood cancer in this cohort.  相似文献   

16.
OBJECTIVE: Our purpose was to assess the risk of ectopic pregnancy among women who smoke cigarettes. STUDY DESIGN: We used data from a case-control study of ectopic pregnancy conducted from October 1988 to August 1990 at an inner-city hospital in Georgia. Cases were 196 non-Hispanic black women with a surgically confirmed ectopic pregnancy. Controls were non-Hispanic black women who had delivered either a live or a stillborn infant weighing at least 500 gm (n = 882) or who were pregnant and seeking an induced abortion (n = 237). RESULTS: After we adjusted for parity, douching history, history of infertility, and age, the odds ratio for ectopic pregnancy was 1.9 (95% confidence interval 1.4 to 2.7) for women who smoked during the periconception period compared with women who did not smoke at that time. After stratification by the amount of daily smoking during the periconception period, the odds ratio rose from 1.6 (95% confidence interval 0.9 to 2.9) for women who smoked 1 to 5 cigarettes to 1.7 (95% confidence interval 1.1 to 2.8) for women who smoked 6 to 10 cigarettes to 2.3 (95% confidence interval 1.3 to 4.0) for women who smoked 11 to 20 cigarettes, and to 3.5 (95% confidence interval 1.4 to 8.6) for women who smoked >20 cigarettes per day. CONCLUSION: In this inner-city population, cigarette smoking was an independent, dose-related risk factor for ectopic pregnancy among black women. The public health and medical care communities should inform the public of this additional risk associated with cigarette smoking and intensify intervention strategies to reduce cigarette smoking among women of reproductive age.  相似文献   

17.
This study compared stable very light smokers ([VLS]; less than 6 cigarettes a day) with regular smokers ([RS]; greater than 14 cigarettes a day) in a cohort of women followed up for 1 yr. The VLS showed evidence of inhaling the cigarette smoke. They were not novice smokers, nor were they under particular pressure to limit their smoking. Among the 61 VLS, 34 had at one time smoked more than 10 cigarettes per day. These "reduced smokers" were broadly similar to the lifetime VLS, who differed from RS in several important respects. In a multiple logistic regression, education and smoking patterns in relatives were independently associated with very light versus regular smoking. Familial factors and personal resources may protect against dependence among those who use tobacco. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

18.
BACKGROUND: According to the American Heart Association, passive smoking is an important risk factor for coronary heart disease (CHD), but the mechanisms underlying this association are not fully understood. We studied the acute effect of passive smoking on the factors that influence the development of CHD: the antioxidant defense of human serum, the extent of lipid peroxidation, and the accumulation of LDL cholesterol in cultured human macrophages, the precursors of foam cells in atherosclerotic lesions. METHODS AND RESULTS: Blood samples were collected during 2 ordinary working days from healthy, nonsmoking subjects (n=10) before and after (up to 5.5 hours) spending half an hour in a smoke-free area (day 1) or in a room for smokers (day 2). Passive smoking caused an acute decrease (1.5 hours after exposure) in serum ascorbic acid (P<.001) and in serum antioxidant defense (P<.001), a decreased capacity of LDL to resist oxidation (P<.01), and the appearance of increased amounts of lipid peroxidation end products in serum (P<.01). Finally, LDL isolated from subjects after passive smoking was taken up by cultured macrophages at an increased rate (P<.05). CONCLUSIONS: Exposure of nonsmoking subjects to secondhand smoke breaks down the serum antioxidant defense, leading to accelerated lipid peroxidation, LDL modification, and accumulation of LDL cholesterol in human macrophages. These data provide the pathophysiological background for the recent epidemiological evidence about the increased CHD risk among passive smokers.  相似文献   

19.
Because of the strong association of active smoking with fetal growth retardation, increasing interest has focused on whether there is also an association with exposure to environmental tobacco smoke (ETS). We examined this issue in a retrospective study and by conducting a review of the literature and data pooling. In our study, nonsmoking women with singleton livebirths born in 1986-87 (n = 992) provided information on exposure to ETS for 1 h or more per day and paternal smoking. The risk of low birthweight (LBW, < 2500 g) was not increased in infants of ETS-exposed women, but there was a somewhat increased risk for LBW at term (adjusted odds ratio [OR] 1.8, 95% confidence interval [CI] 0.6, 4.8) and small-for-gestational-age (< 10th percentile of weight; OR = 1.4, 95% CI = 0.8, 2.5). These results were in the range of 16 other studies in the literature that had odds ratios from 1.0 to 2.2. A weighted average of the results of all studies on LBW at term or small-for-gestational-age yielded a pooled estimate of 1.2 [95% CI = 1.1, 1.3] in nonsmoking women. The pooled estimate of mean birthweight indicated a decrement of 28 g with ETS exposure of nonsmoking women [95% CI = -41, -16], with a greater decrement (about 40 g) seen among more homogeneous studies.  相似文献   

20.
BACKGROUND: A systematic quantitative review of the evidence relating parental smoking to the prevalence of asthma and respiratory symptoms was conducted amongst school age children. METHODS: Sixty relevant studies were identified after consideration of 1593 articles selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search was completed in April 1997 and identified 25 studies of asthma, 41 of wheeze, 34 of chronic cough, seven of chronic phlegm and six of breathlessness which were included in a quantitative overview. RESULTS: The pooled odds ratios for either parent smoking were 1.21 (95% CI 1.10 to 1.34) for asthma, 1.24 (95% CI 1.17 to 1.31) for wheeze, 1.40 (95% CI 1.27 to 1.53) for cough, 1.35 (95% CI 1.13 to 1.62) for phlegm, and 1.31 (95% CI 1.08 to 1.59) for breathlessness. Adjustment for confounding had little effect. Evidence of heterogeneity between studies appeared largely explicable by publication bias with a superfluity of small studies with large odds ratios. However, excluding these had little effect on the pooled odds ratios. The prevalence of all symptoms increased with the number of parents who smoked. While maternal smoking had a greater effect than paternal smoking, the effect of father only was clearly significant. CONCLUSIONS: The relationship between parental smoking and respiratory symptoms seems very likely to be causal given statistical significance, robustness to adjustment for confounding factors, consistency of the findings in different countries, and evidence of dose response. The raised risk in households where the father, but not the mother, smoked argues for a postnatal effect.  相似文献   

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