Influence on fetal growth of exposure to tobacco smoke during pregnancy

We analysed the effect of exposure to tobacco smoke during pregnancy on fetal growth parameters in 129 term newborns. Children were classified into four depending on exposure on the basis of a questionnaire completed by the mother. The results confirmed that tobacco smoking reduced weight, length, cranial and thoracic perimeters at birth when exposure was due to either active or passive smoking. Weight deficits of infants whose mothers smoked heavily (458 g) were higher than those whose mothers were exposed to passive smoking (192 g). We conclude that passive smoking is a very important variable and should be taken into account in any study of neonatal growth parameters.     

Prevention of cardiovascular disease in women: Role of the obstetrician-gynecologist

Cardiovascular disease poses a major threat to women's health. Obstetrician-gynecologists dominate the adult health care field in preventive services in the United States, and the scope of their preventive services should be broadened to encompass cardiovascular disease in women. Endogenous and exogenous risk factors jointly conyribute to a woman's cardiovascular risk profile; the risk of cardiovascular disease should be viewed as a multifactorial phenomenon with a continuous gradient of response. Three important risk factors—serum cholesterol, hypertension, and cigarette smoking—are amenable to change and should become a principal focus of women's health care. Although preventive medicine lacks the glamour and immediate rewards of obstetric and gynecologic interventions, the long-term benefits to the health of women are compelling.     

Airway reactivity response to aged carbon-graphite/epoxy composite material smoke

Exposure of na&ıuml;ve guinea pigs for a total of 30 min to aged smoke from pyrolysis of 5, 10 and 100 g of carbon–graphite/epoxy‐advanced composite material (cgeCM) elicited changes in the ventilation and breathing pattern reminiscent of an acute, asthmatic episode. The severity of these responses was dose related. Although breathing pattern changes were not definitive of stimulation by a single type of respiratory irritant, non‐dimensional indices derived from breath structure appeared to be characteristic of bronchoconstriction possibly complicated by CO₂‐stimulated ventilation. The highest exposure concentration also elicited convulsions in the animals, which may or may not be related to the airway reactivity (AR) response. Upon treatment with fresh air, breathing returned to normal. However, this recovery was transient with some respiratory parameters returning to abnormal levels, possibly indicating a rebound or delayed component of the response. Filtration of particulate material from the smoke moderated but did not eliminate the AR response. Animals exposed to diluted smoke from the pyrolysis of 2 g of cgeCM showed no remarkable changes in breathing or ventilation, suggesting that there may be a threshold for aged cgeCM smoke‐elicited AR response. Published in 2002 by John Wiley & Sons, Ltd.     

Cigarette smoking and subsequent risk of lung cancer by histologic type in middle-aged Japanese men and women: the JPHC study

In order to update the findings of relative risk associated with cigarette smoking for lung cancer by histologic type in Japan, the data from a population-based cohort study of 91,738 men and women were analyzed. During 1990-1999, 422 lung cancer incident cases were identified. The relative risk for all incident cases associated with current smokers versus non-smokers was 4.5 [95% confidence interval (CI): 3.0-6.8] and 4.2 (95% CI: 2.4-7.2), for men and women, respectively. When divided by histologic type, relative risk for squamous cell carcinoma and small cell carcinoma was 12.7 (95% CI: 4.7-34.7) and 17.5 (95% CI: 4.9-62.1), while for adenocarcinoma it was 2.8 (95% CI: 1.6-4.9) and 2.0 (95% CI: 0.8-5.0) for men and women, respectively. We confirmed that the lung cancer risk in men rose with increasing cigarette smoking, especially the duration of smoking among current smokers and decreased after the cessation of smoking among former smokers. Unlike the US or European countries, the relative risk did not increase in this updated study, compared with previous studies in 1960s to 1990s in Japan either for all incident cases or for specific histologic types and the magnitude of relative risks was substantially lower than that observed in the US or European countries, especially for adenocarcinoma.     

Cigarette smoking,alcohol consumption and subsequent gastric cancer risk by subsite and histologic type

The effect of cigarette smoking or alcohol consumption on the risk of gastric cancer has not been clarified. We investigated this relationship, considering the anatomic subsite and histologic type of gastric cancer. A total of 19,657 men (aged 40-59 years at baseline), who responded to the baseline questionnaire and reported no serious illness at that time, were followed for 10 years, from January 1990 to December 1999. Gastric cancer was confirmed histologically in 293 men. Smoking was associated with an increased risk of the differentiated type of distal gastric cancer; compared to the group who never smoked, the adjusted rate ratios (RRs) of gastric cancer for past and current smokers were 2.0 (95% CI 1.1-3.7) and 2.1 (95% CI 1.2-3.6), respectively. No association was observed between cigarette smoking and risk of the undifferentiated type of distal gastric cancer except for a suggestive association with cardia cancer. For alcohol consumption, elevated risk was suggested only for cardia cancer of all histologic types, though the relationship failed to reach significance. Among those who drank alcohol at least once per week, RRs for ethanol intake of 2.7-161.0, 162.0-322.0 and 322.5+ g/week compared to those who drank 0-3 times/month were 2.5 (95% CI 0.7-9.5), 3.3 (0.9-11.6) and 3.0 (0.8-11.1), respectively (p(trend) = 0.66). In conclusion, our results confirm that smoking is related to gastric cancer of the differentiated type. Further studies with more cases are needed to detect a positive association between cigarette smoking or alcohol consumption and cardia cancer.     

A prospective cohort study of cigarette smoking and pancreatic cancer in Japan

Objective: To examine the association of cigarette smoking with the risk of death from pancreatic cancer in a prospective cohort study. Methods: A total of 110,792 inhabitants, aged 40–79 years (46,465 men and 64,327 women), were enrolled from 1988 to 1990 and followed up for mortality to the end of 1997. At baseline a self-administered questionnaire was used to obtain information on cigarette smoking and other lifestyle factors. Results: During the follow-up period (mean ± SD: 8.1 ± 1.8 years), 225 deaths due to pancreatic cancer were identified. After adjustment for age, body mass index, history of diabetes mellitus, and gallbladder diseases, the relative risks (RRs) for current smokers were 1.6 (95% CI 0.95–2.6) in males, and 1.7 (95% CI: 0.84–3.3) in females. Men who smoked more than 40 cigarettes per day had a substantially higher risk of pancreatic cancer, with a RR of 3.3 (95% CI: 1.4–8.1). A significantly decreasing trend in risk with increasing years after smoking cessation was observed (trend p = 0.04) among male ex-smokers. The RRs were 0.85 (95% CI 0.36–2.0) and 0.85 (0.36–2.0) for those who had quit smoking for 10–19 and 20 years, respectively. Conclusions: Our cohort study confirmed that cigarette smoking was associated with an increased risk of death from pancreatic cancer.     

被动吸烟对儿童免疫功能的影响

目的研究被动吸烟对儿童免疫功能的影响.方法于2002-2004年对广州市某小学135名10～11岁儿童的家庭成员吸烟情况及儿童因病缺勤状况进行问卷调查,并对其中50名儿童进行血清IgE和IL-8浓度的检测.结果被动吸烟(n=30)儿童的血清IgE浓度高于非被动吸烟组(n=20),而其IL-8浓度低于非被动吸烟组(P均＜0.05).被动吸烟儿童(n=67)因病缺勤率高于非被动吸烟儿童(n=68),差异有统计学意义(P＜0.05),且多为呼吸系统炎症.结论被动吸烟对儿童的先天性和获得性免疫功能均有不良的影响,应采取有效措施减少儿童被动吸烟的暴露.     

Issues in Design and Implementation in an Urban Birth Cohort Study: The Syracuse AUDIT Project

The Syracuse AUDIT (Assessment of Urban Dwellings for Indoor Toxics) project is a birth cohort study of wheezing in the first year of life in a low-income urban setting. Such studies are important because of the documented serious risks to children's health and the lack of attention and published work on asthma development and intervention in communities of this size. We studied 103 infants of mothers with asthma, living predominantly in inner-city households. Our study combines measurements of a large panel of indoor environmental agents, in-home infant assessments, and review of all prenatal and postnatal medical records through the first year of life. We found multiple environmental pollution sources and potential health risks in study homes including high infant exposure to tobacco smoke. The prevalence of maternal smoking during pregnancy was 54%; postnatal environmental tobacco smoke (ETS) exposure was nearly 90%. The majority (73%) of homes showed signs of dampness. Participants' lives were complicated by poverty, unemployment and single-parenthood. Thirty-three percent of fathers were not involved with their children, and 62% of subjects moved at least once during the study period. These socioeconomic issues had an impact on project implementation and led to modification of study eligibility criteria. Extensive outreach, follow up, and relationship-building were required in order to recruit and retain families and resulted in considerable work overload for study staff. Our experiences implementing the project will inform further studies on this and other similar populations. Future reports on this cohort will address the role of multiple environmental variables and their effects on wheezing outcome during the first year of life.Crawford, Hargrave, Liu, Anbar, Hall, Naishadham, Czerwinski, Webster, Lane, and Abraham are with the Department of Pathology, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA; Hunt is with the UNYSPEC Ltd., Baldwinsville, NY, USA.     

肺癌组织中FHIT基因蛋白的表达缺失与吸烟的关系

目的；研究脆性组氨酸三联体（FHIT）基因蛋白在肺癌组织中的表达及其与吸烟的关系。方法：运用免疫组织化学SP法检测56例外科切除的肺癌组织中FHIT蛋白的表达。结果：56例肺癌组织中33例（58.9%)显示FHIT蛋白缺失。肺鳞癌（SqCCs)中FHIT蛋白缺失率明显高于非鳞癌（non-SqCCs)(72.7% vs39.1%;x^2=6.32,P=0.012)；而且吸烟患者中FHIT蛋白缺失率明显高于非吸烟者（67.5%Vs37.5%;x^2=4.25,P=0.039）。结论：FHIT蛋白的表达缺失是肺癌中的常发事件，尤其在肺鳞癌和吸烟者中。FHIT蛋白的表达可以作为肺癌诊断的一个标志物，FHIT基因可能在吸烟相关的肺癌形成过程中起一定作用。     

Perinatal exposure to environmental tobacco smoke induces adenylyl cyclase and alters receptor-mediated cell signaling in brain and heart of neonatal rats

Perinatal exposure to environmental tobacco smoke (ETS) has adverse effects on neurobehavioral development. In the current study, rats were exposed to ETS during gestation, during the early neonatal period, or both. Brains and hearts were examined for alterations in adenylyl cyclase (AC) activity and for changes in beta-adrenergic and m2-muscarinic cholinergic receptors and their linkage to AC. ETS exposure elicited induction of total AC activity as monitored with the direct enzymatic stimulant, forskolin. In the brain, the specific coupling of beta-adrenergic receptors to AC was inhibited in the ETS groups, despite a normal complement of beta-receptor binding sites. In the heart, ETS evoked a decrease in m2-receptor expression. In both tissues, the effects of postnatal ETS, mimicking passive smoking, were equivalent to (AC) or greater than (m2-receptors) those seen with prenatal ETS mimicking active smoking; the effects of combined prenatal and postnatal exposure were equivalent to those seen with postnatal exposure alone. These data indicate that ETS exposure evokes changes in cell signaling that recapitulate those caused by developmental nicotine treatment. Since alterations in AC signaling are known to affect cardiorespiratory function, the present results provide a mechanistic link reinforcing the participation of ETS exposure, including postnatal ETS, in disturbances culminating in events like Sudden Infant Death Syndrome.