Influence Of Environmental Tobacco Smoke Research Articles

ASTHMA AND RESPIRATORY SYMPTOMS RELATED TO THE ENVIRONMENT

Asthma, a ubiquitous chronic respiratory ailment, stands as a formidable global health concern, affecting millions of individuals across the world. This widespread condition, marked by airway inflammation and heightened reactivity, has captured the attention of researchers and healthcare professionals alike for decades. Its intricate etiology, influenced by a myriad of factors, has fueled the curiosity of the scientific community. As we delve deeper into the annals of medical research, an increasingly compelling narrative emerges—one that underscores the pivotal role played by environmental factors in the development and exacerbation of asthma. At its core, asthma represents a complex interplay between genetic predisposition and environmental exposures. While genetics undoubtedly confer a degree of susceptibility, the multifactorial nature of this condition beckons us to explore the environmental determinants that often act as catalysts for its onset. This comprehensive research paper, therefore, seeks to unravel the multifaceted relationship between asthma and the environment. In doing so, it endeavors to provide valuable insights into the mechanisms by which environmental exposures may contribute to the susceptibility, prevalence, and severity of asthma, ultimately influencing the health and well-being of countless individuals worldwide. Asthma, in its clinical presentation, reflects a state of heightened airway reactivity and inflammation. These hallmark features result in recurrent episodes of wheezing, coughing, shortness of breath, and chest tightness. These symptoms, while variable in intensity and duration, can significantly disrupt the lives of those afflicted. Yet, beyond its clinical manifestations, asthma's origins lie embedded in the intricate web of environmental exposures that individuals encounter throughout their lives. Air quality emerges as a paramount concern in the context of asthma. Airborne pollutants, including fine particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and volatile organic compounds (VOCs), are pervasive in urban and industrialized settings. Substantial evidence from epidemiological studies and clinical research has underscored their association with asthma incidence and symptom exacerbation. These pollutants infiltrate the respiratory system, provoking inflammation and airway hyper responsiveness, thus serving as key triggers for asthma attacks. Furthermore, the indoor environment, where individuals spend a significant portion of their lives, carries its own set of challenges. Allergen exposure, particularly to house dust mites, pet dander, and mold, constitutes a prominent risk factor for asthma. In genetically predisposed individuals, exposure to these allergens can initiate and perpetuate chronic airway inflammation, leading to the characteristic symptoms of asthma. Notably, the interplay between genetic susceptibility and environmental exposures becomes apparent in the variable responses observed among individuals exposed to the same allergenic triggers. The relationship between asthma and environmental factors extends beyond pollutants and allergens. Climate and weather patterns play a noteworthy role, influencing the prevalence and severity of asthma symptoms. Changes in temperature, humidity levels, and pollen counts can lead to fluctuations in asthma exacerbations. For many asthma sufferers, specific seasons bring heightened risks, as increased pollen levels during spring or summer can trigger allergic responses and exacerbate airway inflammation. The influence of environmental tobacco smoke, both in utero and during childhood, looms large as well. Exposure to tobacco smoke is known to augment the risk of developing asthma and exacerbate symptoms in those already afflicted. The harmful constituents of tobacco smoke exert detrimental effects on lung development, immune function, and airway reactivity, further entwining environmental exposures with asthma pathogenesis. In the quest to understand the intricate relationship between asthma and the environment, the paper recognize the heterogeneity of asthma. This condition manifests in various phenotypes, each characterized by unique clinical features and underlying mechanisms. Environmental factors do not exert a uniform influence; rather, they interact with an individual's genetic makeup to produce a nuanced clinical profile. This diversity underscores the complexity of asthma research and the need for personalized approaches to prevention and management.

Influência da fumaça do cigarro na etiologia do linfoma em gatos domésticos

Neoplasms correspond to the large part of routine care of domestic animals, and, among them, lymphoma represents the tumor with the highest incidence in domestic cats. Due to its multifactorial etiology, being influenced by environmental factors and lifestyles of the animals, we raised the hypothesis that exposure to tobacco smoke influences the development of lymphoma in domestic cats. These animals are very close to the guardians, in addition to hygiene habits (grooming), which favors the inhalation of smoke and ingestion of tobacco particles that are deposited in the fur. According to studies, domestic cats exposed to tobacco smoke have higher risks of developing lymphoma when compared to non-exposed cats, and this higher index is directly related to the components found in smoke. Nicotine, cotinine and NNAL(4-(methylnitrosamine)-1-(3-pyridil)-1-butanone) are the main metabolites derived from tobacco and they have been used as urinary biomarkers. Studies show that domestic cats that live in households with the presence of smokers present relevant levels of urinary biomarkers when compared to animals not exposed to environments with smokers. Nicotine levels in animals are directly proportional to the number of cigarettes smoked by guardians and are related to the degree of exposure of animals. Based on epidemiological research, exposure to smoke is related to the emergence of neoplasms in domestic cats similar to that in humans, but it is necessary to develop new research in the veterinary area.

Influence of Environmental Tobacco Smoke and Air Pollution on Fetal Growth: A Prospective Study.

Exposure to air pollution during pregnancy leads to adverse pregnancy outcomes. Few studies have evaluated the influences of air quality, including environmental tobacco smoke (ETS) and particulate matter (PM), on fetal development, which this study examined. This longitudinal correlation study used multiple linear regression data analysis of PM2.5/PM10, self-reported ETS exposure, urinary cotinine level, maternal characteristics, and birth parameters (gestational week, body weight, body length, head, and chest circumferences) with the effect of air quality on fetal growth. The study included 74 pregnant women (mean age 31.9 ± 4.2 years, body mass index 23.6 ± 3.8 kg/m2, average gestational duration 38.5 ± 0.8 weeks). ETS exposure decreased birth length by ≥1 cm, and potentially is an independent risk factor for fetal growth restriction, and pregnant women should avoid indoor and outdoor ETS. However, neither PM2.5/PM10 nor ETS was associated with low birth weight or small for gestational age. This study adds to the evidence base that ETS exposure of nonsmoking pregnant women affects the fetal birth length. Family members should refrain from smoking near expectant mothers, although smoking in the vicinity of their residential surroundings potentially exposes mothers and their fetuses to ETS. Public pollution and childbirth education classes should include details of indoor ETS.

Metabolomics reveals effects of maternal smoking on endogenous metabolites from lipid metabolism in cord blood of newborns.

Introduction A general detrimental effect of smoking during pregnancy on the health of newborn children is well-documented, but the detailed mechanisms remain elusive.Objectives Beside the specific influence of environmental tobacco smoke derived toxicants on developmental regulation the impact on the metabolism of newborn children is of particular interest, first as a general marker of foetal development and second due to its potential predictive value for the later occurrence of metabolic diseases.MethodsTobacco smoke exposure information from a questionnaire was confirmed by measuring the smoking related metabolites S-Phenyl mercapturic acid, S-Benzyl mercapturic acid and cotinine in maternal urine by LC–MS/MS. The impact of smoking on maternal endogenous serum metabolome and children’s cord blood metabolome was assessed in a targeted analysis of 163 metabolites by an LC–MS/MS based assay. The anti-oxidative status of maternal serum samples was analysed by chemoluminiscence based method.ResultsHere we present for the first time results of a metabolomic assessment of the cordblood of 40 children and their mothers. Several analytes from the group of phosphatidylcholines, namely PCaaC28:1, PCaaC32:3, PCaeC30:1, PCaeC32:2, PCaeC40:1, and sphingomyelin SM C26:0, differed significantly in mothers and children’s sera depending on smoking status. In serum of smoking mothers the antioxidative capacity of water soluble compounds was not significantly changed while there was a significant decrease in the lipid fraction.ConclusionOur data give evidence that smoking during pregnancy alters both the maternal and children’s metabolome. Whether the different pattern found in adults compared to newborn children could be related to different disease outcomes should be in the focus of future studies.Electronic supplementary materialThe online version of this article (doi:10.1007/s11306-016-0983-z) contains supplementary material, which is available to authorized users.

Exposure to environmental tobacco smoke and respiratory tract infections in pre-school children – a cross-sectional study in Poland

Knowledge of the harmful influence of environmental tobacco smoke (ETS) has a positive impact on changing social behaviours worldwide. In many homes smoking is totally prohibited; in some others, partial limitations of tobacco consumption have been introduced. To study the correlation between the adopted rules of tobacco use in homes of 3-year-olds, and the kind and frequency of acute respiratory system infections within a 6-month period of attending pre-schools. The study was performed among children attending municipal pre-schools in Białystok, Poland. The data was collected by anonymous questionnaires completed by the parents of 302 children aged 3 years chosen randomly from 1,200 children attending 51 pre-schools. The exposure of children to tobacco smoke was measured by determining cotinine to creatinine ratio (CCR) in urine. In the 150 families of children who were surveyed, 210 were smokers. Every day, the smokers consisted of fathers (37.3%) and mothers (23.6%). The 3-year-old children were divided into 3 groups according to smoking habits in their homes: 28.5% of the children under examination came from homes where tobacco smoking was forbidden (mean CCR - 15.21 ng/mg, SD=11.86), 26.2% came from homes where tobacco was smoked in separate rooms (mean CCR - 65.75 ng/ml, SD=81.51), 45.4% lived in homes where no rules connected with smoking had been established (mean CCR - 61.75 ng/ml, SD= 70.29). During the analyzed period of 6 months, 85% of the children had at least 1 respiratory tract infection (60% - upper, 16.9% - lower, 16.5% - upper and lower, 7.1% - otitis media). The majority of the 3-year-old children who had lower respiratory tract infections required antibiotics and hospitalization. Living in a home where no tobacco rules were established may cause an increase of respiratory tract infections.

Exposure determinants of cadmium in European mothers and their children

The metal cadmium (Cd) is a widespread environmental pollutant with documented adverse effects on the kidneys and bones from long-term environmental exposure, but with insufficiently elucidated public health consequences such as risk of cardiovascular disease, hormone-related cancer in adults and developmental effects in children. This study is the first pan-European human biomonitoring project that succeeded in performing harmonized measurements of Cd in urine in a comparable way in mother–child couples from 16 European countries. The aim of the study was to evaluate the overall Cd exposure and significant determinants of Cd exposure.A study population of 1632 women (24–52 years of age), and 1689 children (5–12 years of age), from 32 rural and urban areas, was examined within a core period of 6 months in 2011–2012. Women were stratified as smokers and non-smokers. As expected, smoking mothers had higher geometric mean (gm) urinary cadmium (UCd; 0.24µg/g crea; n=360) than non-smoking mothers (gm 0.18µg/g crea; n=1272; p<0.0001), and children had lower UCd (gm 0.065µg/g crea; n=1689) than their mothers at the country level. Non-smoking women exposed to environmental tobacco smoke (ETS) at home had 14% (95% CI 1–28%) higher UCd than those who were not exposed to ETS at home (p=0.04). No influence of ETS at home or other places on UCd levels was detected in children. Smoking women with primary education as the highest educational level of the household had 48% (95% CI 18–86%) higher UCd than those with tertiary education (p=0.0008). The same observation was seen in non-smoking women and in children; however they were not statistically significant. In children, living in a rural area was associated with 7% (95% CI 1–13%) higher UCd (p=0.03) compared to living in an urban area. Children, 9–12 years had 7% (95% CI 1–13%) higher UCd (p=0.04) than children 5–8 years.About 1% of the mothers, and 0.06% of the children, exceeded the tolerable weekly intake (TWI) appointed by EFSA, corresponding to 1.0µgCd/g crea in urine. Poland had the highest UCd in comparison between the 16 countries, while Denmark had the lowest. Whether the differences between countries are related to differences in the degree of environmental Cd contamination or to differences in lifestyle, socioeconomic status or dietary patterns is not clear.

Association of tobacco smoke exposure and atopic sensitization

BackgroundForty million children are regularly exposed to environmental tobacco smoke (ETS) each year, increasing their risk for premature death and middle ear and acute respiratory infections. Early life exposure to ETS also is clearly associated with wheezing. However, there is no clear understanding of the influence of ETS on the development of allergic sensitization. ObjectiveTo determine the association of combined exposure to ETS and indoor allergens on IgE sensitization to aeroallergens in children. MethodsThis case–control study enrolled 116 cases and 121 controls from low-income families from Kansas City, Missouri. The adjusted odds ratio was calculated using a logistic model to assess the association between ETS and allergic sensitization using dust allergen levels as a covariate. ResultsThirty-six percent of atopic children and 39% of controls were exposed to ETS (P < .05). Unadjusted analyses showed no significant influence of ETS on IgE sensitization to indoor allergens. Logistic regression analyses also showed no significant influence of ETS on sensitization when adjusted for levels of allergens in the home dust and family history of allergic rhinitis. ConclusionThese data suggest that ETS exposure was not associated with IgE sensitization to indoor allergens, even when home allergen levels were taken into consideration. Further understanding of how components of tobacco smoke influence the immune response is necessary to interpret the disparate findings across studies.

Environmental Tobacco Smoke Induces Oxidative Stress in Distinct Brain Regions of Infant Mice

Environmental tobacco smoke (ETS) leads to the death of 600,000 nonsmokers annually and is associated with disturbances in antioxidant enzyme capacity in the adult rodent brain. However, little is known regarding the influence of ETS on brain development. The aim of this study was to determine levels of malonaldehyde (MDA) and 3-nitrotyrosine (3-NT), as well as enzymatic antioxidant activities of glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), and superoxide dismutase (SOD), in distinct brain structures. BALB/c mice were exposed to ETS twice daily for 1 h from postnatal day 5 through postnatal day 18. Acute exposure was performed for 1 h on postnatal day 18. Mice were euthanized either immediately (0) or 3 h after the last exposure. Immediately after an acute exposure there were higher GR and GST activities and MDA levels in the hippocampus, higher GPx and SOD activities in the prefrontal cortex, and higher GST activity and MDA levels in the striatum and cerebellum. Three hours later there was an increase in SOD activity and MDA levels in the hippocampus and a decrease in the activity of all enzymes in the prefrontal cortex. Immediately after final repeated exposure there were elevated levels of GST and GR activity and decreased GPx activity in the hippocampus. Moreover, a rise was found in GPx and GST activities in the prefrontal cortex and increased GST and GPx activity in the striatum and cerebellum, respectively. After 3 h the prefrontal cortex showed elevated GR and GST activities, and the striatum displayed enhanced GST activity. Data showed that enzymatic antioxidant system in the central nervous system responds to ETS differently in different regions of the brain and that a form of adaptation occurs after several days of exposure.

Influence of environmental tobacco smoke on characteristics of childhood asthma

We compared characteristics of asthma in children from smoking and non-smoking families. To examine if there was any difference in asthma in children exposed and not exposed to environmental tobacco smoke (ETS). We examined 231 asthmatic children and their parents. According to the questionnaire and carbon monoxide (CO) values in exhaled air measured by Smokerlyzer, we divided the children in two groups: children from smoking and children from non-smoking families. We compared birth weight, birth length, the occurrence of the first broncho-obstruction, the number of respiratory infections and exacerbations per year, asthma severity, the number of hospitalizations, total IgE, Skin prick test and allergic manifestations. We examined the influence of parental educational level on smoking behaviour and how much money a smoking family spent on cigarettes. The children's average age was 10.6 years, there were 49% of boys and 51% of girls. We had 77% of smoking families, 45.9% of active smoking mothers and 51% of active smoking fathers. Smoking was more common among lower educated parents. A smoking family spent 7.3% of the family budget on cigarettes. The children from smoking families had more allergic manifestations. The children of smoking mothers had more respiratory infections (without a statistic difference in the second and third year) and more asthmatic exacerbations with a statistic difference after the third year. With parents who smoked, children had more severe asthma. There was no statistical difference in the following: birth weight, birth length, Skin prick test, total IgE, the first wheezing episode and the number of hospitalizations. However, in the group of 26 children with exhaled CO values higher than 6 ppm, birth weight was lower (3250 g vs. 3550 g), the first wheezing episode occurred earlier (2 years vs. 3.7 years) and total IgE was higher (702 IU/ml vs. 563 IU/ml) by more than two normal ranges (60 IU/ml). It is necessary to protect children with asthma from ETS because it has a negative impact on their illness.

Urinary 1-hydroxypyrene in children living in city and rural residences in Denmark

Aims The present study aims to assess the biological uptake in children of polycyclic aromatic hydrocarbons measured as 1-hydroxypyrene in urine from children living in city and rural residences. Methods 103 children living in Copenhagen and 101 children living in rural residences of Denmark collected urine samples Monday to Friday morning. Each day, the family filled in a printed diary that included questions about the time and activity patterns of the child. Multiple regression analyses were used to identify predictors of the excreted 1-hydroxypyrene level. Results During the week, the children excreted on average 0.07 [95% CI: 0.01–0.41] μmol urinary 1-hydroxypyrene per mol creatinine. Children living in urban residences excreted 0.02 [95% CI: 0.01–0.05] μmol more 1-hydroxypyrene than children living in rural residences. This was confirmed in the multiple regression analysis showing a 29% (95% CI: 2–64%) higher excretion among urban children than rural children. Moreover, the regression analysis showed that for each hour per day spent outside the children excreted 58% (1.58 [1.22–2.03]) more 1-hydroxypyrene in urine. Conclusion The present study indicates that children living in urban residences are more exposed to PAH than children living in rural residences. Time spent outdoors increased the excretion of 1-hydroxypyrene, which was most evident among urban children. Higher concentrations of ambient air pollution in urban areas may explain this finding. No influence of environmental tobacco smoke, cooking habits, and heating facilities was detected.

Urinary 1-hydroxypyrene in children living in city and rural residences in Denmark

Aims The present study aims to assess the biological uptake in children of polycyclic aromatic hydrocarbons measured as 1-hydroxypyrene in urine from children living in city and rural residences. Methods 103 children living in Copenhagen and 101 children living in rural residences of Denmark collected urine samples Monday to Friday morning. Each day, the family filled in a printed diary that included questions about the time and activity patterns of the child. Multiple regression analyses were used to identify predictors of the excreted 1-hydroxypyrene level. Results During the week, the children excreted on average 0.07 [95% CI: 0.01–0.41] μmol urinary 1-hydroxypyrene per mol creatinine. Children living in urban residences excreted 0.02 [95% CI: 0.01–0.05] μmol more 1-hydroxypyrene than children living in rural residences. This was confirmed in the multiple regression analysis showing a 29% (95% CI: 2–64%) higher excretion among urban children than rural children. Moreover, the regression analysis showed that for each hour per day spent outside the children excreted 58% (1.58 [1.22–2.03]) more 1-hydroxypyrene in urine. Conclusion The present study indicates that children living in urban residences are more exposed to PAH than children living in rural residences. Time spent outdoors increased the excretion of 1-hydroxypyrene, which was most evident among urban children. Higher concentrations of ambient air pollution in urban areas may explain this finding. No influence of environmental tobacco smoke, cooking habits, and heating facilities was detected.

Acute exposure to environmental tobacco smoke reduces HDL-C and HDL 2-C

Background. Chronic environmental tobacco smoke (ETS) exposure increases individuals risk of coronary artery disease by reducing high-density lipoprotein cholesterol (HDL-C). Currently, there is limited research on the acute effects of ETS on HDL-C. This study examined the acute influence of ETS on HDL-C and its subfractions. Methods. Twelve male subjects (25.7 ± 3.0 years) were examined to determine the influence of an acute 6-h exposure to ETS on lipid and lipoprotein levels. Baseline blood samples were drawn before ETS exposure from an antecubital vein at 6 am, 2 pm, and 10 pm. The following day, subjects were exposed to 6 h of ETS, approximately 4–10 pm. Blood was again collected at 8, 16 and 24 h following ETS exposure. Blood was assayed for total cholesterol (TC), HDL-C and its subfractions HDL 2-C and HDL 3-C. Results. As a result of ETS exposure, HDL-C and HDL 2-C levels were significantly reduced by 18% and 37%, respectively. This effect was sustained, with a decrease in HDL-C of 13% and HDL 2-C of 28% still evident at 24-h post-exposure. TC was unchanged (pre- 187.3 ± 41.6 and post- 187.0 ± 46.3); however, there were significant decreases in the TC/HDL-C and HDL 2-C/HDL 3-C ratios by 16% and 29%, respectively, which were sustained for 24 h. Conclusions. The findings of this study demonstrate that a 6-h exposure has a negative impact on lipid and lipoprotein profiles and that these levels remained depressed for at least 24 h.

Influence of environmental tobacco smoke on vitamin C status in children

It is known that vitamin C status is compromised in smokers. The vitamin C status of nonsmokers who are exposed to environmental tobacco smoke (ETS) is now being elucidated. We assessed vitamin C status in children who were either exposed or not exposed to ETS, and we sought to associate changes in vitamin C status with the amount of ETS exposure. The study group included 512 children aged 2-12 y; 50% of them were exposed to ETS in the home because their parents smoked. Dietary intake of vitamin C, obtained with a 24-h recall questionnaire, and blood ascorbate concentrations were compared in the exposed and unexposed groups. Smoke exposure was assessed by measuring a biomarker, urinary cotinine. Age, sex, and body mass index were examined as potential correlates of vitamin C status in each exposure category. Plasma ascorbate concentrations were lower, by 3.2 micro mol/L on average, in ETS-exposed children than in unexposed children who consumed equivalent amounts of vitamin C; this was a highly significant difference (P = 0.002). This reduction in plasma ascorbate occurred even with very low exposure to ETS. ETS can reduce concentrations of ascorbate, an important blood antioxidant, even when the amount of smoke exposure is minimal. Children exposed to ETS should be encouraged to consume increased amounts of foods rich in vitamin C or should be given the equivalent amount of this vitamin as a supplement.

Secondhand Smoke Induces Allergic Sensitization in Mice

Purpose of the Study. Although there is evidence that environmental tobacco smoke (ETS) can exacerbate allergic responses, the role of ETS in primary allergic sensitization remains unclear. The objective of this study was to examine the influence of ETS on allergic sensitization in a mouse model.Study Population. Female BALB/c and C57BL/6 mice.Methods. The investigators exposed mice to either ovalbumin (OVA), saline, ETS, or OVA + ETS by nebulization. Total IgE and OVA-specific immunoglobulin E (IgE), IgG1 and IgG2a were quantified for each of the 4 exposure groups. Mice were reexposed to nebulized OVA 30 days after the initial exposure and cytokine levels in bronchoalveolar lavage (BAL) fluid were measured. Interleukin (IL)-2, IL-4, IL-5, IFN-γ and granulocyte-macrophage colony-stimulating factor (GM-CSF) were measured to look for evidence of Th1 or Th2 skewed immune responses. Two strains of mice were studied, BALB/c, a high IgE producer, and C57BL/6, a low IgE producer.Results. An allergic antibody response, as measured by total IgE and OVA-specific IgE and IgG1, was present in C57BL/6 mice exposed to OVA + ETS, but was not detectable in those exposed to saline, OVA alone, or ETS alone. The results were statistically significant. The allergic antibody response in the BALB/c mice was also most pronounced in the group exposed to OVA + ETS. As this strain more readily produces IgE, there was detectable total IgE as well as OVA-specific IgE and IgG1 in the group exposed to OVA alone, but levels of OVA-specific IgE and IgG1 were statistically significantly higher in the OVA + ETS group. BAL fluid was examined for eosinophilia after rechallenge with OVA in C57BL/6 mice. The OVA + ETS group had marked eosonophilia while the saline, OVA and ETS groups had no eosinophils. Cytokines were also quantified in BAL fluid. IFN-γ, a Th1-associated cytokine, was decreased in OVA + ETS mice as compared with the OVA-exposed group (P < .01), while IL-5, a Th2-associated cytokine, was increased as compared with the OVA-exposed group (P < .05).Conclusion. ETS exposure appears to facilitate the primary allergic response in mice as measured by allergic antibody response and BAL cytokine response and eosinophilia.Reviewers’ Comments. Although some evidence has been published regarding ETS and its role in exacerbating allergic responses, this is the first study demonstrating a significant role for ETS in primary allergic sensitization in mice. Future studies will no doubt address the applicability of these findings to humans.

Geographical distribution of benzene in air in northwestern Italy and personal exposure.

Benzene is a solvent strictly related to some industrial activities and to automotive emissions. After the reduction in lead content of fuel gasoline, and the consequent decrease in octane number, an increase in benzene and other aromatic hydrocarbons in gasoline occurred. Therefore, an increase in the concentration of these chemicals in the air as primary pollutants and as precursors of photochemical smog could occur in the future. The objectives of this study were to describe the benzene air pollution at three sites in northwestern Italy throughout 1991 and 1994; to examine the relationship between benzene air pollution in indoor, outdoor, and personal air as measured by a group of nonsmoking university students; and to determine the influence of environmental tobacco smoke on the level of benzene exposure in indoor air environments. The results indicate a direct relationship between population density and levels of contamination; an indoor/outdoor ratio of benzene air pollution higher than 1 during day and night; a similar level of personal and indoor air contamination; and a direct relationship between levels of personal exposure to benzene and intensity of exposure to tobacco smoke. Human exposure to airborne benzene has been found to depend principally on indoor air contamination not only in the home but also in many other confined environments.

Influence of Environmental Tobacco Smoke on Asthma in Nonallergic and Allergic Children

The relation between past induced abortions and subsequent fetal loss is still unclear. We report a case-control study with 331 cases of first spontaneous abortion and 993 controls with no previous spontaneous abortion and a normal pregnancy at the same period of pregnancy. In comparison with primigravid women, the odds ratio for a fetal loss in the current one was 1.41 [95% confidence interval (CI) = 0.81-2.43] among women with one previous pregnancy ending in induced abortion, 4.43 (95% CI = 1.46-13.36) among those with two previous induced abortions out of two pregnancies, and 1.35 (95% CI = 0.64-2.82) among women with three or more previous pregnancies ending in one or more induced abortions.

Influence of worksite environmental tobacco smoke on serum lipoprotein profiles of female nonsmokers

The purpose of this study was to examine the influence of environmental tobacco smoke (ETS) in the workplace on high-density lipoprotein cholesterol (HDL-C), HDL-C subfractions, and apolipoprotein (apo) A-I and apo B in female workers. Premenopausal women free from factors known to influence HDL-C (cigarette smoking, vigorous physical exercise, etc) who were not taking oral contraceptives, were moderate consumers of alcohol, caffeine, and dietary fat, and were between the ages of 21 and 50 years participated in one of two groups: (1) nonsmokers who had never smoked cigarettes and were generally free from ETS exposure (nonsmokers), and (2) nonsmokers who had never smoked but were subjected to concentrated doses of ETS at least 6 hours per day, 4 days per week, for at least the past 6 consecutive months (ETS-exposed). A third group consisting of current cigarette smokers who smoked a minimum of 20 cigarettes per day for at least the past 5 consecutive years served as smoking controls (smokers). Subjects were matched by group as closely as possible with regard to criteria that can influence blood lipoprotein levels. Participants were solicited from taverns and restaurants where they were employed. It was hypothesized that individuals chronically exposed to ETS would demonstrate unfavorable lipoprotein profiles. Results showed that HDL-C, HDL 2, and apo A-I were significantly ( P < .05) depressed for ETS-exposed and smokers as compared with nonsmokers. Values for ETS-exposed were not different from those for smokers. Total cholesterol, triglycerides, HDL 3, and apo B did not differ among the three groups. It was concluded that excessive exposure to ETS in female workers can have deleterious effects on HDL-C, HDL 2, and apo A-I in nonsmokers that are similar to effects observed in cigarette smokers. It is possible that these effects increase coronary artery disease (CAD) risk.

Benzene, toluene and xylenes in air, geographical distribution in the Piedmont region (Italy) and personal exposure

The objectives of this study were the determination of: (a) benzene (B), toluene (T) and xylene (X) air pollution in three sites of the Piedmont region (north-western Italy), (b) the relationship between BTX pollution in indoor, outdoor and personal air measured for a group of non-smoking university students, (c) the influence of environmental tobacco smoke on the level of BTX exposure for indoor air environments. Results indicate (i) a direct relationship between human density and level of contamination and higher toluene pollution, (ii) an indoor/outdoor ratio of > 1 for all the three aromatics, (iii) a similar level of personal and indoor air contamination. Human exposure to BTX air pollution has been found to depend principally on indoor air contamination, not only on home pollution, but also, probably on many other confined environments.