Passive smoking and risk of cancer

During the last two decades there have been frequent discussions as to whether passive smoking causes cancer, or not. It is difficult to carry out satisfactory studies on this issue, partially because any increased risk of cancer seems modest. The tobacco industry has not only attempted to make the public aware of studies which conclude that passive smoking is harmless, but it has also tried to keep alive the discussion as to whether exposure to passive smoking is harmful, or not. A large number of studies has been carried out on the possible impact passive smoking may have on the risk of lung cancer, and it seems justifiable to conclude that passive smoking does increase the risk of this type of cancer. For other types of cancer too few studies have been performed to draw any firm conclusions.     

Passive smoking in children up to 5 years of age

Passive smoking is a major health risk in young children. We investigated the percentage of children with mothers and/or fathers who reported regular smoking. Data are the national and regional health surveys of the German Cardiovascular Prevention Study (GCP) conducted from 1984 to 1992 in West Germany. 2538 mothers aged 25-40 years were included. The prevalence of passive smoking in children due to smoking mothers was 33.6% 55.4% of the children up to 5 years lived in households with at least one smoking parent member. In 23.4% of these households both parents were smokers. If only one member of the parents smoked this was in two out of three cases the father. 28.2% of mothers with a child younger than one year were current smokers. This prevalence rate increased with the age of the youngest child up to 35.6% for mothers, whose youngest child was 5 years old. Multiple logistic regression analysis was performed to investigate the association between smoking behaviour and the following variables: mother's age, social class, family status, community size and year of the survey. It was found that lower social class members, unmarried or divorced mothers and inhabitants of large cities reported significantly more often regular current smoking. These results underscore the importance of special intervention programs to reduce smoking in parents with young children.     

Passive cigarette smoking and reduced HDL cholesterol levels in children with high-risk lipid profiles

BACKGROUND: HDL cholesterol levels are known to be lower in smokers than in nonsmokers. Previous studies have demonstrated an association of decreased HDL cholesterol with passive smoking in children but have not adjusted for potential confounding factors. METHODS AND RESULTS: In a cross-sectional, pilot-scale study, we examined the relationship of HDL cholesterol levels to passive smoking in children and adolescents referred to a tertiary hyperlipidemia clinic. Eligibility criteria included (1) first visit to a lipid clinic, (2) LDL cholesterol >95th percentile for age or HDL cholesterol <5th percentile, (3) age between 2 and 18 years, and (4) absence of secondary causes of hyperlipidemia. Sociodemographic information, diet record, medical history, and fasting lipid profiles were obtained. Of 109 eligible patients, 103 (94%) were studied. Twenty-seven percent came from households with cigarette smokers. HDL cholesterol levels were 38.7+/-1.2 mg/dL (mean+/-SEM) in passive smokers versus 43.6+/-1.2 mg/dL in children without smoke exposure (P=.005). Smoking exposure was not significantly associated with other lipid values. The effect of smoking on HDL cholesterol was minimally affected by potential confounders. In multivariate regression adjusting for body mass index, age, sex, exercise, and dietary fat intake, passive smoking remained a significant risk factor for decreased HDL cholesterol (P=.012). CONCLUSIONS: Mean HDL cholesterol levels are lower in dyslipidemic children from households with smokers than in those without household smoke exposure. Passive smoking may worsen the risk profile for later atherosclerosis among high-risk young persons.     

Health effects of passive smoking. 8. Passive smoking and risk of adult asthma and COPD: an update

Chronic ingestion of ethanol produces a variety of effects on female reproductive function, depending on the dose and the exposure time but the mechanism of alcohol-induced ovarian failure has been little studied. Also the effects of chronic ethanol consumption on the oocyte quality in relation to morphological alterations and PGE synthesis by the oocyte cumulus complexes (OCCs) have not been described. In this study, immature female mice were treated with 10% ethanol in drinking water for 30 days. Then they were induced to superovulate, and at 14, 16 and 20 h post-hCG the quality of the ovarian and oviductal oocytes and PGE production by OCC was determined. At 14 h post-hCG, the percentage of oviductal immature oocytes was increased in the ethanol-treated females (P < 0.05). At 16 h post-hCG, the percent of oviductal activated oocytes was higher in the treated females (P < 0.05), and the ovarian immature oocytes were decreased as compared to the control females (P < 0.05). At 20 h post-hCG, the ethanol-treated females had higher percents of activated oocytes in the oviducts and in the ovaries (P < 0.05) with respect to the controls. PGE synthesis by OCCs, assessed by RIA, was decreased in the treated female mice (P < 0.001). In summary, moderate chronic ethanol treatment in immature female mice can produce morphologic abnormalities in the oocytes (high parthenogenetic activated rates) and altered PGE production in the OCCs.     

Passive smoking and plasma fibrinogen concentrations

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.     

Tolerance of pyrazinamide in short course chemotherapy for pulmonary tuberculosis in children

BACKGROUND: This prospective study was performed to evaluate the tolerance of pyrazinamide in short course chemotherapy in children. METHODS: A total of 114 children ages 6 months to 15 years (4.5 +/- 3.4 years) with diagnosed pulmonary tuberculosis from 1985 to 1995 entered the trial. A 2-month regimen of isoniazid, rifampin and pyrazinamide, followed by rifampin and isoniazid for the remaining 4 months, was administered orally to all children. Clinical adverse effects specifically investigated were gastrointestinal disturbances, rash, signs of hepatotoxicity and arthralgias. Laboratory toxicity data (number of leukocytes, erythrocyte sedimentation rate, aspartate aminotransferase, alanine aminotransferase and serum uric acid) were collected before treatment and 1, 3 and 5 months after the beginning of chemotherapy. RESULTS: Clinical adverse effects were mild in all cases. Three children (2.6%) had fever and 5 (4.4%) had gastrointestinal disturbances. Aspartate aminotransferase and alanine aminotransferase mean values showed no differences along time and no patients had clinical signs of hepatotoxicity. Only 11 children (19.6%) showed a slight increase in alanine aminotransferase (< 194 units/l). Serum uric acid increased in 92.2% of the children compared with pretreatment values. This increase remained within the normal range in all but 9.8% of patients. There was a significant increase in uric acid mean concentrations after 1 month of therapy (from 3.7 +/- 0.7 mg/dl to 5.7 +/- 1.6 mg/dl, P < 0.05), which fell again (4.0 +/- 1.1) 1 month after pyrazinamide was stopped. There were no signs of gout or arthralgias. In no case was the treatment interrupted. CONCLUSION: The addition of pyrazinamide in chemotherapy for pulmonary tuberculosis in children was found to be safe. The slight increase in uric acid concentration during its administration had no recognized adverse consequences.     

Passive smoking induces atherogenic changes in low-density lipoprotein

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.     

Cigarette smoking by mothers during pregnancy and pulmonary function of their school age children

The paper examines the relation of maternal smoking during pregnancy and lung function of 1029 schoolchildren aged 9 years. Children from Cracow whose mothers had smoked during pregnancy had significantly lower lung function than the children whose mothers had not smoked in this period. On average, spirometric data of FEV1/FVC, FEF25-75% and PEFR were 1.1%, 4.7%, and 3.2% lower respectively, in those children whose mothers had smoked during pregnancy. The effect was statistically significant after accounting for potential confounders such as current smoking habit of parents. The results provide a new support for the hypothesis that deficit in lung function among children is associated with maternal smoking in pregnancy. The strongest effects were found to involve the function of small airways.     

Parental smoking and risk factors for cardiovascular disease in 10- to 12-year-old children

Combined alteration of the pyruvate dehydrogenase complex and respiratory chain function is described in a 21 year-old male patient with overlapping MELAS (mitochondrial encephalomyopathy, lactic acidosis, and 'stroke-like' episodes) and Kearns-Sayre syndrome. Progressive external ophthalmoplegia, pigmentary retinopathy and right bundle branch block were present when he experienced the first 'stroke-like' episode at 18 years old. The A>G tRNALeu(UUR) point mutation at nucleotide 3243 of the mitochondrial DNA was predominant in muscle tissue (79%) and present, but at lower levels in fibroblasts (49%) and blood cells (37%). Biochemical analysis revealed diminished activities of pyruvate dehydrogenase (23%) and respiratory chain complexes I and IV (57%, respectively) in muscle, but normal activities in the fibroblasts. Immunochemical studies of the muscular pyruvate dehydrogenase components showed normal content of E1alpha, E1beta and E2 protein. Molecular screening of the E1alpha gene did not indicate a nuclear mutation. These observations suggest that mitochondrial DNA defects may be associated with altered nuclear encoded enzymes which are actively imported into mitochondria and constitute components of the mitochondrial matrix. Biochemical workup of mitochondrial disorders should not be restricted to the respiratory chain even if mitochondrial DNA mutations are present.     

Passive smoking, active smoking, and education: their relationship to weight history in women in Geneva

OBJECTIVES: This study was undertaken to determine the relationship of education and tobacco smoke to lifetime weight history in women. METHODS: Information on passive smoking, active smoking, and weight history was collected from 928 women aged 29 to 74 years selected from the general population of Geneva, Switzerland. Multivariate analysis of variance was performed for weight, weight at age 20, and weight changes since age 20. RESULTS: Education was inversely related to weight at age 20, current weight, and weight gain since age 20. The least educated group had a current weight of 4 kg more than the most educated group. Differences across smoking categories were small: passive smokers had the highest current weight (63.4 kg) and former active smokers had the lowest (60.4 kg). Weight gain since age 20 tended to be smaller in former and current active smokers (5.5 to 7.2 kg) than in passive smokers (8.3 to 10.4 kg) and those never exposed (9.1 kg). CONCLUSIONS: In this sample, education was an important predictor of women's current weight and weight history. Passive and active smoking had little long-term effect on weight.     

Predictive factors of Mycobacterium tuberculosis infection and pulmonary tuberculosis in prisoners

BACKGROUND: Tuberculosis currently represents a serious problem in prison populations. METHODS: With the aim of studying the predictive factors for, and the prevalence of, Mycobacterium tuberculosis infection and pulmonary tuberculosis in a Spanish prison, all those admitted during 1991 and 1992 were included (N = 1314). The tuberculin skin test, HIV serology, chest X-ray and bacteriological examination of sputum were carried out. Statistical analysis was done by univariant tests, stratified analysis and logistic regression. RESULTS: The prevalence of M. tuberculosis infection was 55.5% (95% confidence interval [CI] 52.5-58.5). An association was found with sex, imprisonment more than once, HIV infection and age. The co-infection rate (tuberculosis plus HIV) was 9.2%. Logistic regression showed a greater risk with age (4.4% per year), time spent in prison and for males. The prevalence of pulmonary tuberculosis was 1.26% and an association was found with M. tuberculosis infection, HIV infection (odds ratio [OR] = 13.7), intravenous drug users (OR = 17.2) and imprisonment more than once (OR = 7.3). Logistic regression showed an association with HIV co-infection (OR = 20.2). CONCLUSIONS: The prevalence of M. tuberculosis infection and pulmonary tuberculosis is high when compared with similar studies. The influence of age, time spent in prison and co-infection with HIV is relevant to recommendations for specific tuberculosis prevention programmes in correctional facilities.