Article

Hjern A, Hedberg A, Haglund B, Rosen MDoes tobacco smoke prevent atopic disorders? A study of two generations of Swedish residents. Clin Exp Allergy 31:908-914

Authors:
To read the full-text of this research, you can request a copy directly from the authors.

Abstract

Earlier studies have given conflicting results regarding the effect of exposure to tobacco smoke on atopic sensibilization. A cross-sectional study of present and former smoking habits in relation to atopic disorders from data on 6909 young and middle-aged adults (16-49 years) and their 4472 children (3-15 years) from the Swedish Survey of Living Conditions in 1996-97. The prevalence of allergic asthma and allergic rhino-conjunctivitis decreased, in a dose-response manner (P = 0.03 and P = 0.004, respectively), with increasing exposure to tobacco smoke in the adult study population. This pattern was little changed when potential confounders (sex, age, education, domicile, country of birth) were entered into a multivariate analysis: the adjusted odds ratio (OR) for allergic rhino-conjunctivitis was 0.5 (0.4-0.7) for those who smoked at least 20 cigarettes a day and OR 0.7 (0.6-0.9) for those smoking 10-19 cigarettes, compared with those who reported that they never had smoked Former smokers had a tendency for a slightly lower risk: OR 0.9 (0.8-1.0). In a multivariate analysis, children of mothers who smoked at least 15 cigarettes a day tended to have lower odds for suffering from allergic rhino-conjunctivitis, allergic asthma, atopic eczema and food allergy, compared to children of mothers who had never smoked (ORs 0.6-0.7). Children of fathers who had smoked at least 15 cigarettes a day had a similar tendency (ORs 0.7-0.9). This study demonstrates an association between current exposure to tobacco smoke and a low risk for atopic disorders in smokers themselves and a similar tendency in their children. There is a need for further studies with a prospective design to certify the causal direction of this association. Smoking habits and atopic disorder in parents should not be considered independent variables in epidemiological studies of the connection between exposure to tobacco smoke and atopy in children.

No full-text available

Request Full-text Paper PDF

To read the full-text of this research,
you can request a copy directly from the authors.

... It is noteworthy that some studies reached similar conclusions as ours [9,16,35,36], and some of them (e.g., the one of Linneberg and colleagues [35]) were also prospective birth cohort studies. In line with our results, the study of Hjern et al. reported that parental tobacco smoking was a protective factor even after controlling for confounding factors such as sex, age, and socioeconomic factors [36]. ...
... It is noteworthy that some studies reached similar conclusions as ours [9,16,35,36], and some of them (e.g., the one of Linneberg and colleagues [35]) were also prospective birth cohort studies. In line with our results, the study of Hjern et al. reported that parental tobacco smoking was a protective factor even after controlling for confounding factors such as sex, age, and socioeconomic factors [36]. Ludvigsson et al. reported that parental smoking was associated with a lower risk of AD, and their conclusion was reinforced by urine cotinine measurements in part of the study population [16]. ...
... To explain the unexpected finding of a negative association between passive smoking and AD, most authors brought up residual confounding [9,35,36], but to date, this has not been investigated in detail. It is conceivable that smokers may have specific behaviors that could be protective against AD development, such as ventilating the housing more frequently or going for a walk outside with the infant while smoking [36]. ...
Article
Full-text available
The influence of environmental factors on atopic dermatitis (AD) has been investigated in many cross-sectional studies. It remains however unclear if they could influence AD development early in life. This prospective birth cohort study aimed to monitor aspects of family lifestyle and child’s nutrition within a Caucasian population and to assess its association with AD development over the first 2 years of life. Genetic predisposition was evaluated based on family history and profilaggrin genotyping. Of 149 included children, 36 developed AD. Infants with a family history of atopy developed AD 2.6 times more frequently (30 of 97) than infants without atopic predisposition (6 of 52). Genotyping was carried out on 50% of the children included. Profilaggrin mutations (R501X, 2282del4, R2447X, and S3247X) were infrequent in our population. Lower incidence of AD was observed in infants exposed to a damp housing environment, lower household income, and smoking mothers with a higher but not with a lower education level.Conclusion: Family history of atopy was a significant risk factor for AD regardless of the most common, currently defined, FLG mutations. Humidity at home and passive smoking seem associated with AD development in infancy. What is Known: • Atopic dermatitis (AD) is associated with mutations in various genes of the immune system and the epidermal barrier complex in particular filaggrin (FLG) mutation. • Inherited factors alone cannot explain the rising AD; environmental factors are therefore likely to play a decisive role in this rise but the exact role that these factors may play in increasing AD risk in infancy remains unclear. Moreover, the relationship between environmental factors and AD has been the focus of mostly cross-sectional studies and not prospective studies. What is New: • This prospective birth cohort study demonstrates that family history of atopy is a significant risk factor for AD regardless of the most common, currently defined, FLG mutations. • A lower incidence of AD was observed in infants exposed to a moist housing environment, lower household income, and smoking of mothers with a higher but not with a lower education level.
... Some studies have shown an association between current CS exposure and a low risk for allergic rhinitis (Hjern et al., 2001;Nagata et al., 2008) and that the prevalence of allergic asthma and allergic rhinitis decreased with increased exposure to CS (Hjern et al., 2001). Conversely, CS reportedly increases nasal allergic responses with concomitant increase in the serum immunoglobin E (IgE) level and production of interleukin-5 (IL-5) (Oryszczyn et al., 2000;Saulyte et al., 2014;Kim et al., 2017). ...
... Some studies have shown an association between current CS exposure and a low risk for allergic rhinitis (Hjern et al., 2001;Nagata et al., 2008) and that the prevalence of allergic asthma and allergic rhinitis decreased with increased exposure to CS (Hjern et al., 2001). Conversely, CS reportedly increases nasal allergic responses with concomitant increase in the serum immunoglobin E (IgE) level and production of interleukin-5 (IL-5) (Oryszczyn et al., 2000;Saulyte et al., 2014;Kim et al., 2017). ...
... Many previous reports have revealed that CS could augment allergic inflammation (Botelho et al., 2011;Saulyte et al., 2014;Strzelak et al., 2018); however, chronic smoking exerts a protective effect on allergic sensitization to some aeroallergens and prevents allergic diseases protecting against pollinosis (Hjern et al., 2001;Sopori, 2002;Nagata et al., 2008;Monico et al., 2019). Various components of CS suppress the Th2 cell response, which plays an important role in IgE production and in the development of immediate hypersensitivity (Ozaki et al., 2010), although the mechanism by which CS protects against allergic sensitization has not been well clarified. ...
Article
Full-text available
Objective Cigarette smoke (CS) exposure reportedly enhances allergic airway inflammation. However, some studies have shown an association between current cigarette smoke exposure and a low risk for allergic rhinitis. Thus, the impact of CS exposure on allergic rhinitis remains poorly understood. The purpose of this study was to investigate the effects of CS on the respiratory mucosa (RM) and the olfactory epithelium (OE) of mice with allergic rhinitis, as the effects may differ depending on the nasal histological compartments. Methods Eight-week-old male BALB/c mice were used for this study. We developed a mouse model of smoking by intranasally administering 10 doses of a CS solution (CSS), and a mouse model of allergic rhinitis by sensitization with intraperitoneal ovalbumin (OVA) injection and intranasal challenge with OVA. We examined the effects of CS on the nasal RM and OE in mice with or without allergic rhinitis using histological, serum, and genetic analyses. First, we examine whether CSS exposure induces allergic responses and then, examined allergic responses in the OVA-sensitized allergic rhinitis mice with or without CSS exposure. Results Short-term CSS administration intensified allergic responses including increased infiltration of eosinophils and inflammatory cells and upregulation of interleukin-5 expression in the nasal RM of OVA-immunized mice, although only CSS induced neither allergic responses nor impairment of the RM and OE. Notably, repetitive OVA-immunization partially impaired the OE in the upper-lateral area, but CSS administration did not reinforce this impairment in OVA-induced allergic mice. Conclusion Short-term CSS exposure strengthened allergic responses in the nasal RM and did not change the structure of the OE. These results suggest that patients with allergic rhinitis could experience exacerbation of allergic symptoms after CS exposure.
... Previous population studies on the association between tobacco smoking and allergic rhinitis have provided diverse results [43, 47, 54,130131132133134135136137138. Most studies have found a lower prevalence of allergic rhinitis in smokers than in non-smokers [43, 47, 54,130131132133134135136, but there are also reports of the opposite [137, 138]. ...
... Previous population studies on the association between tobacco smoking and allergic rhinitis have provided diverse results [43, 47, 54,130131132133134135136137138. Most studies have found a lower prevalence of allergic rhinitis in smokers than in non-smokers [43, 47, 54,130131132133134135136, but there are also reports of the opposite [137, 138]. Population-based studies on the association between smoking and chronic rhinitis are few, but have consistently found an increased risk in smokers compared to non-smokers [49, 139, 140]. ...
... Although it is well known that smoking increases lung function decline [141] and disease morbidity in subjects with asthma [142, 143], the impact of smoking on asthma development is still a matter of debate. Most crosssectional studies have not found smoking to be associated with asthma [136, 144, 145], while ex-smoking has occasionally been associated [146, 147]. Various studies of case-referent and prospective design have reported significant associations between smoking and development of asthma in adults [ ...
Thesis
Full-text available
The prevalence of rhinitis and asthma has increased considerably over the past century. The cause of this increase remains unknown. Furthermore, rhinitis and asthma are now considered heterogeneous syndromes encompassing several clinical phenotypes. The overall aim of this thesis was to investigate the prevalence, risk factors and comorbidity of rhinitis and asthma phenotypes with a particular focus on aspirin-intolerant asthma. This thesis is mainly based on a postal questionnaire with 18 087 responders (62%) living in West Sweden. The prevalence of allergic rhinitis (AR) was 20% in those raised on a farm compared to 28% in subjects raised elsewhere. A lower prevalence of AR in subjects raised on a farm was found in all age groups. The prevalence of chronic rhinitis (CR) was 20%. Both AR and CR were more common in urban than in rural areas. Cigarette smoking was associated with a high prevalence of CR and a low prevalence of AR. Both associations were dose-dependent and were found also in two large population surveys conducted in the city of Stockholm. Skin prick testing was performed on a randomly selected subsample of the West Sweden cohort. Prevalence of skin prick test positivity was significantly lower in smokers (34%) than in non-smokers (46%). Considerable overlap was found between asthma and nasal comorbidities and different nasal comorbidities were associated with different symptom expression of asthma. Prevalence of aspirin-intolerant asthma (AIA) was 0.5%. The risk of AIA increased linearly with increasing body mass index. CR was commonly found in AIA. We conclude that AR and CR are common in the general population of West Sweden. The two rhinitis phenotypes share some, but not all, risk factors. Both conditions are associated with asthma and lower respiratory symptoms, indicating a strong relationship between the upper and lower airways. Aspirin-intolerant asthma was found in the general population as was associated with obesity and chronic rhinitis.
... Čini se da bi sinergistički učinak ranije opisivanih promjena imunološkog sustava, povećane propusnosti sluznice oštećene duhanskim dimom čime je omogućena penetracija raznih potencijalnih alergena mogao biti uzrokom povećane učestalosti atopijskih oboljenja kod djece pasivnih pušača. No, valja naglasiti da postoje istraživanja koja nisu dokazala povećanu incidenciju atopijskih oboljenja kod pasivnih pušača iako je učinak bio izraženiji kod odraslih nego kod djece (48). Veliko švedsko istraživanje je pokazalo da je kod odraslih prevalencija alergijske astme i alergijskog rinokonjuktivitisa niža kod onih koji su izloženi pasivnom pušenju, a sličan je učinak iako slabije izražen, utvrđen i kod djece izložene duhanskom dimu njihovih roditelja otvarajući kontroverzno pitanje mogućeg protektivnog učinka (48). ...
... No, valja naglasiti da postoje istraživanja koja nisu dokazala povećanu incidenciju atopijskih oboljenja kod pasivnih pušača iako je učinak bio izraženiji kod odraslih nego kod djece (48). Veliko švedsko istraživanje je pokazalo da je kod odraslih prevalencija alergijske astme i alergijskog rinokonjuktivitisa niža kod onih koji su izloženi pasivnom pušenju, a sličan je učinak iako slabije izražen, utvrđen i kod djece izložene duhanskom dimu njihovih roditelja otvarajući kontroverzno pitanje mogućeg protektivnog učinka (48). No, najnovija istraživanja su pokazala da genski polimor fi zmi u antioksidativnoj aktivnosti pridonose razlikama u osjetljivosti na učinke duhanskog dima, pretpostavljajući da bi upravo genske razlike bile uzrokom dobivenih različitih rezultata istraživanja odnosa pasivne izloženosti duhanskom dimu i učinaka na dišni sustav pasivnih pušača (49). ...
Article
Full-text available
Although many investigations have noted harmful effects of passive smoking on respiratory health of children, a great proportion of parents continue smoking and exposing their children to tobacco smoke. The main objective of this review is to highlight the harmful effects of passive exposure to tobacco smoke on the respiratory system in children and to identify the possible mechanisms of development of these disorders. It has been demonstrated that passive exposure to tobacco smoke is a significant risk factor for respiratory tract infections; it was found to reduce the levels of lung function and increase the incidence of childhood asthma. Several studies have reported that children of smoking parents had a lower grade of motor skills and physical condition than children of non-smoking parents. Children born to mothers that smoked during pregnancy have been shown to have an increased risk of respiratory tract illnesses during childhood. Data on the harmful effects of tobacco smoke should help in launching public health preventive action towards minimizing exposure of children to passive smoking and all detrimental influences of passive smoke exposure on the children’s health.
... The data from one study were obtained from the authors [39]. We found 97 studies on allergic rhinitis [19,21,24,, 91 on allergic dermatitis [19,20,22,[24][25][26][44][45][46]48,53,[60][61][62][63][64][65]67,73,75,76,78,[83][84][85][86][87]91,93,96,97,99,[101][102][103][105][106][107]110,111,, and eight on food allergies [14,23,26,73,126,136,[166][167][168]. ...
... The data from one study were obtained from the authors [39]. We found 97 studies on allergic rhinitis [19,21,24,, 91 on allergic dermatitis [19,20,22,[24][25][26][44][45][46]48,53,[60][61][62][63][64][65]67,73,75,76,78,[83][84][85][86][87]91,93,96,97,99,[101][102][103][105][106][107]110,111,, and eight on food allergies [14,23,26,73,126,136,[166][167][168]. ...
Article
Full-text available
Allergic rhinitis, allergic dermatitis, and food allergy are extremely common diseases, especially among children, and are frequently associated to each other and to asthma. Smoking is a potential risk factor for these conditions, but so far, results from individual studies have been conflicting. The objective of this study was to examine the evidence for an association between active smoking (AS) or passive exposure to secondhand smoke and allergic conditions. We retrieved studies published in any language up to June 30th, 2013 by systematically searching Medline, Embase, the five regional bibliographic databases of the World Health Organization, and ISI-Proceedings databases, by manually examining the references of the original articles and reviews retrieved, and by establishing personal contact with clinical researchers. We included cohort, case-control, and cross-sectional studies reporting odds ratio (OR) or relative risk (RR) estimates and confidence intervals of smoking and allergic conditions, first among the general population and then among children. We retrieved 97 studies on allergic rhinitis, 91 on allergic dermatitis, and eight on food allergy published in 139 different articles. When all studies were analyzed together (showing random effects model results and pooled ORs expressed as RR), allergic rhinitis was not associated with active smoking (pooled RR, 1.02 [95% CI 0.92-1.15]), but was associated with passive smoking (pooled RR 1.10 [95% CI 1.06-1.15]). Allergic dermatitis was associated with both active (pooled RR, 1.21 [95% CI 1.14-1.29]) and passive smoking (pooled RR, 1.07 [95% CI 1.03-1.12]). In children and adolescent, allergic rhinitis was associated with active (pooled RR, 1.40 (95% CI 1.24-1.59) and passive smoking (pooled RR, 1.09 [95% CI 1.04-1.14]). Allergic dermatitis was associated with active (pooled RR, 1.36 [95% CI 1.17-1.46]) and passive smoking (pooled RR, 1.06 [95% CI 1.01-1.11]). Food allergy was associated with SHS (1.43 [1.12-1.83]) when cohort studies only were examined, but not when all studies were combined. The findings are limited by the potential for confounding and bias given that most of the individual studies used a cross-sectional design. Furthermore, the studies showed a high degree of heterogeneity and the exposure and outcome measures were assessed by self-report, which may increase the potential for misclassification. We observed very modest associations between smoking and some allergic diseases among adults. Among children and adolescents, both active and passive exposure to SHS were associated with a modest increased risk for allergic diseases, and passive smoking was associated with an increased risk for food allergy. Additional studies with detailed measurement of exposure and better case definition are needed to further explore the role of smoking in allergic diseases. Please see later in the article for the Editors' Summary.
... 25 We have identified the effect of maternal smoking during pregnancy or during infancy as a significant risk factor for FA + children, but the medical literature still debates on this, with some references mentioning it even as a protective factor. 26 Furthermore, alcohol consumption by pregnant mothers appeared significant, but the possible etiologic connection is unknown, and these outcomes should be further assessed in the future. ...
Article
Full-text available
Introduction and objectives: In order to investigate food allergy's prevalence, risk factors and eating behavior of children with relevant anamnesis, a study was performed in Cypriot primary schools. Patients: A specially composed questionnaire for self-reported adverse reactions to food, created in the context of the EuroPrevall study, was distributed in 13 representative primary schools across the country. Participants were sub-grouped into three groups; healthy (H), those with unconfirmed food hypersensitivity reactions (FA-) and children with a confirmed diagnosis by a physician IgE-mediated food allergy (FA+). Food habits, family health history and lifestyle factors were assessed and groups' outcomes were compared with each other. Results: For the study, 202 questionnaires were completed and returned; 31 children (19 FA- and 12 FA+) reported an adverse food reaction. Significant risk factors for developing FA+ were being the first born or having siblings with asthma, attended a day nursery, but also maternal alcohol drinking during pregnancy, parental smoking and parental occupation in food processing or use of latex gloves. The presence of children in the kitchen during cooking showed a protective role. Dietary habits of FA+ children were significantly diminished in terms of variety and frequency of consumption in comparison to the rest, in which had a greater overlap. Conclusion: Further research is required for the interesting risk or protective factors revealing from the current investigation. The negative effect of food allergy in the dietary habits of food allergic children documented in the literature, is strongly supported herein.
... It is critical to emphasize the chemical composition of tobacco and tobacco smoke is complex which may render CO to be an irrelevant agent [361]. Nevertheless, the Smoker's paradox is an emerging term for the controversial phenomenon where, despite the severe toxicity of cigarettes, smoking may have protective benefits based on the observation of an inverse incidence of diseases such as: acute coronary syndrome mortality [362], ulcerative colitis [358], anxiety and depression [363], obesity [364], pemphigus [366], preeclampsia [367], primary sclerosing cholangitis [368], stroke [369], severe COVID-19 [370], and many other indications [371,[435][436][437][438][439][440][441][442][443][444][445][446][447][448][449][450]. Cigarette smoking may also enhance clopidogrel efficacy [372]. ...
Article
It is estimated that 10% of carbon throughout the cosmos is in the form of carbon monoxide (CO) [1]. Earth’s earliest prebiotic atmosphere included the trinity of gasotransmitters CO, nitric oxide (NO), and hydrogen sulfide (H2S), for which all of life has co-evolved with [2]. Speculation for extraterrestrial life in harsh environments is similarly based on harnessing atmospheric CO as a primary energy source [3]. The history of CO can be loosely traced to mythological and prehistoric origins with fundamental understanding emerging in the middle ages. Ancient literature is focused on CO’s deadly toxicity which is understandable in the context of our primitive relationship with coal and fire. Scientific inquiry into CO appears to have emerged throughout the 1700s followed by chemical and toxicological profiling throughout the 1800s. Despite CO’s ghastly reputation, several of the 18th and 19th century scientists suggested a therapeutic application of CO. Since 2000, the fundamental understanding of CO as a deadly nuisance has undergone a paradigm shift such that CO is now recognized as a neurotransmitter and viable pharmaceutical candidate. This review is intended to provide a brief history on the trace origins pertaining to endogenous formation and therapeutic application of CO.
... These results are consistent with previous reports demonstrating that nicotine suppressed Th2 responses in allergic mouse lungs [30] and concanavalin-Ainduced T cell proliferation in rats [31,32]. It has been reported that current tobacco smokers have a low risk of developing allergic asthma and rhino-conjunctivitis [33]. Nizri et al. [34] reported that α7 nicotinic acetylcholine receptor (nAChR) signals display anti-inflammatory effects mediated by the reduction of NF-κB transcription in T cells. ...
Article
Full-text available
Background: Environmental tobacco smoke (ETS) exposure is recognized as a risk factor for the development of various respiratory diseases. Objective: In this study, the effect of ETS on allergen-immunized and allergen-specific Th2 cell-transferred murine eosinophilic inflammation models and that of cigarette smoke extract (CSE) and nicotine on allergen-induced Th2 cell proliferation and interleukin (IL)-4 production were investigated. Methods: Ovalbumin (OVA)-immunized and OVA-specific Th2 cell-transferred BALB/c mice were exposed to ETS and were challenged with OVA. Then, the number of inflammatory cells in the nasal mucosa and nasal hyperresponsiveness (NHR) were assessed. The effects of CSE and nicotine on the allergen-induced proliferative response of and IL-4 production by Th2 cells were determined in vitro. Results: In OVA-immunized and Th2 cell-transferred mice, allergen-induced NHR and nasal eosinophil infiltration were significantly suppressed by ETS exposure, whereas the accumulation of neutrophils was rather enhanced. Allergen-specific Th2 cell proliferation and IL-4 production were inhibited by coculture with CSE. The same effects were induced by nicotine, though the effect on proliferation was relatively weak. Conclusion: Regardless of its harmful effect, ETS suppresses NHR, probably through the inhibition of Th2 cell responses.
... Nicotine reduces the chance of atopic disorders such as allergic asthma (Hjern et al., 2001) probably by acting as anti-inflammatory agent, and interfering with the inflammation-related disease process, as nicotine has vasoconstrictive effects (Melton 2006). ...
Thesis
Full-text available
Nicotine, a widely abused drug, is readily consumed through the various forms of non-prescription nicotine replacement therapies as well as through tobacco smoking. Amidst concerns of possible neurotoxicity, nicotine has been the subject of potential therapeutic value for the management of neurologic and neurodegenerative diseases in the last decade. This study investigated the effects of nicotine on hippocampal and striatal associated behaviours, microanatomy of the hippocampus and striatum, histochemical demonstration of neuritic plaques formation and acetylcholinesterase (AChE) activities and immunohistochemical analysis of certain hippocampal neurogenic markers; protein Ki-67 (Ki-67), Glial Fibrillary Acidic Protein (GFAP), Neuron Specific Enolase (NSE). Twenty eight adult male Wistar rats weighing between 150-200 g were randomly assigned into 4 groups of 7 rats each. Control group was administered normal saline, while 3 treated groups were administered graded doses of nicotine at 0.25, 2 and 4 mg/kg body weight via subcutaneous injections for 28 days. Results showed significant decrease (p<0.001) in weight gain of all nicotine treated groups compared to control [F=13.92; p<0.0001]. Total food consumed was also significantly reduced (p<0.001), albeit dose dependently, as 2 and 4 mg/kg treatment showed lowered consumption compared to 0.25 mg/kg [F=15.40; p<0.0001]. Nicotine produced convulsive movements within the first few minutes (1-4) of administration at 2 and 4 mg/kg treatments but not at 0.25 mg/kg. However, other hippocampal and striatal associated neurobehaviours were not altered following nicotine administration. Nicotine significantly increased (p<0.001) percentage of neurons showing degenerating features at 2 and 4 mg/kg treatments but not 0.25 mg/kg in both the hippocampus [F=83.30; p<0.0001] and striatum [F=67.13; p<0.0001]. However, 4 mg/kg treatment showed significantly higher percentage of neurons presenting degenerating features compared to 2 mg/kg in both brain regions. Nissl substance staining was only significantly improved in the hippocampus following 0.25 mg/kg treatment [F=17.35; p=0.0007]. Bielschowsky method showed no formation of neuritic plaques both in hippocampus and striatum following nicotine treatments. Nicotine significantly increased (p<0.001) acetylcholinesterase (AChE) activities in both hippocampus [F=32.70; p<0.0001] and striatum [F=53.87; p<0.0001] at 2 and 4 mg/kg treatments but not at 0.25 mg/kg. There was no significant difference in percentage of Ki-67 positive cells following nicotine treatments compared to control. Though, 2 mg/kg treatment was significantly higher (p<0.05) compared to 0.25 and 4 mg/kg treatments [F=4.62; p=0.0371]. No significant difference was observed in percentage of GFAP positive cells following nicotine treatments [F=0.13; p=0.9411]. However, 2 mg/kg treatment significantly increased (p<0.01) percentage of NSE cells compared to control and to other nicotine treatments [F=13.37; p=0.0017]. All nicotine treated groups significantly increased (p<0.001) serum Nitric oxide concentration compared to control [F=12.08; p<0.0001]. The present study has shown that nicotine treatment at higher doses showed likelihood of inducing neurodegenerative changes in the hippocampus and striatum. Also, nicotine treatment at higher doses reduces AChE activities in these regions. This is indicative of an additional modulation of the central cholinergic systems in addition to the well-documented stimulation of nicotine acetylcholine receptors. The study has also revealed that nicotine may possibly enhance neurogenesis at certain doses.
... In random-effects models, AD was associated with active smoking ( Eleven studies examined stratified AD prevalence by the levels of exposure to passive smoking. [23][24][25][26][27][28][29][30][31][32][33] There were no significant associations between AD and exposure to mild (OR 1.21, 95% CI 0.81-1.80) or extensive (OR 1.08, 95% CI 0.74-1.59) ...
Article
Background: Tobacco exposure might be a modifiable risk factor for atopic dermatitis (AD). Objective: We examine the association between AD and exposure to tobacco smoke. Methods: We performed a systematic review and meta-analysis of observational studies (n = 86) in MEDLINE, EMBASE, Scopus, and Cochrane Library (1823-2015). Quality of evidence was assessed using the Newcastle-Ottawa Scale (NOS). A meta-analysis was performed using random-effects models to estimate pooled odds ratios (OR). Subset analyses were performed for different ages (children, adult), regions, study designs (cross-sectional, longitudinal), study sizes (<5000, ≥5000), study quality (NOS score <6, ≥6), and amount of smoking (mild, extensive). Results: A diagnosis of AD was associated with higher odds of active smoking (OR 1.87, 95% confidence interval 1.32-2.63) and exposure to passive smoke (OR 1.18, 95% confidence interval 1.01-1.38), but not maternal smoking during pregnancy (OR 1.06, 95% confidence interval 0.80-1.40). The association between active smoking and AD remained significant in children and adults, all continents studied, and study sizes, but all were cross-sectional designs and had NOS score 6 or greater. Passive smoke was associated with AD in children and adults, cross-sectional studies, South/Central American and African studies, study size less than 5000, and NOS score less than 6. Limitations: AD severity and distribution were not assessed. Conclusions: Active and passive exposure to smoke are associated with increased AD prevalence.
... In our study, we found that active smoking during pregnancy has an effect on the risk for bronchiolitis hospitalization that is dose-dependent. We defined heavy smoking mothers who smoked more than 15 cigarettes/ day, as previously done in another study [34], with the aim to emphasize the effect of a discrete number of cigarettes. The dose-dependency of active smoking during pregnancy was observed also for growth restriction in previous studies [27,35]. ...
Article
Full-text available
Background Tobacco smoke exposure (TSE) is a worldwide health problem and it is considered a risk factor for pregnant women’s and children’s health, particularly for respiratory morbidity during the first year of life. Few significant birth cohort studies on the effect of prenatal TSE via passive and active maternal smoking on the development of severe bronchiolitis in early childhood have been carried out worldwide. Methods From November 2009 to December 2012, newborns born at ≥33 weeks of gestational age (wGA) were recruited in a longitudinal multi-center cohort study in Italy to investigate the effects of prenatal and postnatal TSE, among other risk factors, on bronchiolitis hospitalization and/or death during the first year of life. Results Two thousand two hundred ten newborns enrolled at birth were followed-up during their first year of life. Of these, 120 (5.4 %) were hospitalized for bronchiolitis. No enrolled infants died during the study period. Prenatal passive TSE and maternal active smoking of more than 15 cigarettes/daily are associated to a significant increase of the risk of offspring children hospitalization for bronchiolitis, with an adjHR of 3.5 (CI 1.5–8.1) and of 1.7 (CI 1.1–2.6) respectively. Conclusions These results confirm the detrimental effects of passive TSE and active heavy smoke during pregnancy for infants’ respiratory health, since the exposure significantly increases the risk of hospitalization for bronchiolitis in the first year of life. Electronic supplementary material The online version of this article (doi:10.1186/s12931-015-0312-5) contains supplementary material, which is available to authorized users.
... [23][24][25] An analysis of linked routine data in Sweden by Hjern et al. found that children of mothers who smoked at least 15 cigarettes a day tended to have lower odds for having atopic eczema (OR 0Á73). 26 A large Danish study also showed a tendency towards a protective effect of smoking on hay fever and eczema. 23 To explore this further we pooled the estimates from studies estimating the effect of maternal smoking during pregnancy on eczema risk in children. ...
Article
Full-text available
Background: Atopic dermatitis (eczema) in childhood is socially patterned, with higher incidence in more advantaged populations, but it is unclear what factors explain the social differences. Methods: We estimated odds ratios (OR) for ever having had eczema by age 5 in 14,499 children from the United Kingdom Millennium Cohort Study (MCS) with a focus on maternal, antenatal and early life risk factors and socio-economic circumstances (SEC). Risk factors were explored to assess if they attenuated associations between SECs and eczema. Results: 35.1% of children had ever had eczema by age five. Children of mothers with degree level qualifications compared to no educational qualifications were more likely to have eczema (OR 1.52 95% CI 1.31-1.76) and there was a gradient across the socioeconomic spectrum. Maternal atopy, breastfeeding (1-6 weeks and 6 months or more), introduction of solids under 4 months or cow's milk under 9 months, antibiotic exposure in the first year of life and grime exposure were associated with an increased odds of eczema. Female sex, Pakistani and Bangladeshi ethnicity, smoking during pregnancy, exposure to environmental tobacco smoke and more siblings were associated with reduced odds for eczema. Controlling for maternal, antenatal and early life characteristics (particularly maternal smoking during pregnancy, breast-feeding, and number of siblings) reduced the OR for eczema to 1.26 (95%CI 1.03 to 1.5), in the group with the highest educational qualifications compared to the least. Conclusions: In a representative UK child cohort, eczema was more common in more advantaged children and this was partially explained by early life factors including not smoking during pregnancy, breast-feeding, and fewer siblings. This article is protected by copyright. All rights reserved.
... Several epidemiologic studies have reported that exposure to either firsthand or secondhand cigarette smoke exacerbates asthma symptoms (Hersoug et al., 2010;Jung et al., 2012;Papaioannou et al., 2010;Stapleton et al., 2011) and increases the risk of developing asthma (Hunt et al., 2011;Mitchell et al., 2012;Tsai et al., 2010). However, other studies have reported no increased risk of asthma development in smokers (Mohammad et al., 2013;Siroux et al., 2000), while some have even reported a lowered risk of asthma in smokers compared to non-smokers and ex-smokers (Hjern et al., 2001;Troisi et al., 1995). A similar paradigm has been reported in studies using animal models of allergic asthma and cigarette smoke exposure (Lanckacker et al., 2013;Melgert et al., 2004;Robbins et al., 2005;Thatcher et al., 2008;Trimble et al., 2009). ...
Article
Acrolein (ACR), an α,β-unsaturated aldehyde and a major component of tobacco smoke, is a highly reactive electrophilic respiratory irritant implicated in asthma pathogenesis and severity. However, few studies have directly investigated the influence of ACR exposure on allergen sensitization and pulmonary inflammation. The present study was designed to examine the impact of ACR inhalation on allergic sensitization to the inhaled antigen ovalbumin (OVA), as well as pulmonary inflammation during subsequent OVA challenge. Adult male C57BL/6 mice were exposed to inhaled OVA (1%, 30 min/day, 4 days/week) and/or ACR (5 ppm, 4 h/day, 4 days/week) over 2 weeks and subsequently challenged with aerosolized OVA (1%, 30 min/day) over three consecutive days. Serum anti-OVA IgG1 levels were increased significantly in animals exposed to both OVA and ACR, compared to animals exposed to either OVA or ACR alone. In addition, differential cell counts and histological analysis revealed an increase in BAL neutrophils in animals exposed to both OVA and ACR. However, exposure to both OVA and ACR did not influence mRNA expression of the cytokines il5, il10, il13 or tnfa, but significantly increased mRNA expression of ccl20. Moreover, ACR exposure enhanced lung mRNA levels of il17f and tgfb1, suggesting development of enhanced inhalation tolerance to OVA. Overall, the findings indicate that ACR inhalation can promote airway-mediated sensitization to otherwise innocuous inhaled antigens, such as OVA, but also enhances immune tolerance, thereby favoring neutrophilic airway inflammation.
... The possible explanation could be that cigarette smoking may be reduced in families with asthmatic children. ETS exposure may be negatively associated with asthma, likely through selection mechanisms, especially in cross-sectional designs, which were consistent with some studies in Western countries [38,39]. ...
Article
Full-text available
Background: There is growing evidence suggesting that air pollution is responsible for the increasing prevalence of asthma in Asia. Exposure to indoor or outdoor air pollutants in communities is relevant to the acute exacerbation as well as the prevalence of asthma. Air pollutants emitted from coal combustion in households may exceed those from industrial resources, and control of such air pollution is of great public health importance. Tobacco smoke is prevalent in Asia and partly responsible for asthma morbidities, despite growing awareness of its adverse respiratory effects. Methods/Data base: A review of the literature. Results: In some Asian studies, respiratory symptoms were found to be more prevalent in individuals living near busy roads than in those whose residence was exposed to larger amounts of pollen allergens and less traffic. This suggests that air pollution could be a risk factor for asthma in addition to atopy. Ambient air pollutants at current levels have been shown to have a harmful effect on more susceptible people in several countries. It is possible that the permissible levels of air pollutants are not sufficiently low for the protection of human health. Because cross-sectional studies cannot confirm a causal relationship for various asthma morbidities, the association with known air pollutants remains suggestive. Conclusions: More carefully designed long-term studies are needed to document the causal effects and dose-response relationship between various air pollutants and asthma. Better technology and public policy are needed to help prevent the enormous suffering and human loss associated with air pollution. What has yet to be documented is whether reduced indoor and outdoor pollution will result in decreased asthma morbidity. Studies to investigate this hypothesis are currently under way.
... Cigarette smoking primarily suppresses T-helper lymphocyte type 2 (Th2) cytokine/chemokine responses in the lung [3], and decreases the incidence of atopic sensitization to aeroallergens4567891011. Nevertheless, it is reasonable to assume that smoking affects the response to food allergens differently [12]. For instance, smoking is an important source of exposure to toxic elements such as lead (Pb), which is considered to be associated with increased odds of food sensitization in adults [13], but epidemiological findings are still inconsistent [14,15]. Meanwhile, adipose tissue, an important component of the human body, has been thought to influence the immune system and promote the development of atopic sensitization [16]. ...
Article
Full-text available
It is unclear whether the relationship between cigarette smoking and atopy is mediated by body fat mass, such as the Body Mass Index (BMI). We assessed the mediating role of BMI on the relationship between smoking and atopy in Chinese adults. A hospital-based case-control study of 786 atopic cases and 2771 controls was conducted in adults aged 18 years or older from March 2010 to September 2014 in Harbin, China. Mediation models were used to estimate the indirect effects of smoking on atopic sensitization through BMI. Compared to non-smokers, light smokers and moderate smokers had a lower risk of inhalant allergen sensitization. The indirect effect of smoking and sensitization to aeroallergens were only observed in light smokers (point estimate, -0.026; 95% CI, -0.062 to -0.004). The mediating roles of BMI on the relationships between smoking and other types of allergic sensitization were not statistically significant. BMI appeared to partially mediate the effect of light smoking on sensitization to aeroallergens. However, considering the other harmful health effects of cigarette smoking, the effective method to lower the incidence of atopy would be to decrease body fat mass by physical exercise and employing other more healthy ways of living rather than smoking.
... , 흡연 (Al-Sahab et al., 2008;Hjern, Hedberg, Hagrund, & Rosen, 2001;Nolte, Backer, & Porsbjerg, 2001;Sherril, Halonen, & Burrows, 1994;Wilson & Weis, 2011), 운동 (Kim, 2003;Kim, 1998), 수면 (Reuveni, Chapnick, Tal, & Tarasiuk, 1999;Shirakawa & Morimoto, 1991), 다양한 유형의 스트레스 (Carroll, Balkrishnan, Feldman, Fleischer, & Manuel, 2005;Chida, Hamer, & Steptoe, 2008;King & Wilson, 1991) (Kim, 2003), 본 연구에서 아토피 피부염 유병은 아토피 피부 염의 의사진단이 내려진 경우로 판단하였다("예/아니오"). ...
Article
Full-text available
The aim was to explore the relationship between health status/life style and prevalence of atopic dermatitis in adolescents.
... 24 One study reported a reduced risk of rhinoconjunctivitis for children exposed to parental smoking. 25 Conversely, Gonzalez-Diaz et al. showed that passive smoking is one of the risk factors for both rhinitis and rhinoconjunctivitis. 26 More recently, we found that ETS is a significant risk factor for rhinoconjunctivitis. 8 Similarly, a study by Montefort et al. reported that smoking by the mother alone was more common in children having current rhinitis, while smoking by the mother and/or father led to rhinoconjunctivitis. 27 We also found that an increased frequency of high reported truck traffic in the residential streets was an independent risk factor for the association between rhinitis and conjunctivitis (OR 1.57). Although evidence exists that allergic respiratory disorders are associated with traffic exposure in children, the findings are not consistent. ...
Article
Full-text available
Rhinitis and conjunctivitis are common diseases worldwide that are frequently associated. Nevertheless, the risk factors for rhinoconjunctivitis are not well-described and the impact of conjunctivitis on rhinitis and asthma in children remains unknown. This study explored the different risk factors and evaluated the burden of rhinoconjunctivitis among adolescents. This was a cross-sectional study conducted on a random sample of schoolchildren, aged 10-17 years, using skin prick tests and a self-administered questionnaire on respiratory health investigating the impact of rhinitis and rhinoconjunctivitis on daily activities. A complete evaluation was obtained for 2,150 children. The prevalence of rhinitis alone was 18.2% and rhinitis associated with conjunctivitis was 20.5%. Rhinoconjunctivitis was more frequently associated with females, a parental history of atopy, domestic exposure to mold/dampness, passive smoke exposure, and reported truck traffic in residential streets. Moreover, rhinoconjunctivitis was associated with a higher level of allergic sensitization. The prevalence of current asthma was 1.7% in subjects without rhinitis or rhinoconjunctivitis, 5.1% in rhinitis and 10.7% in rhinoconjunctivitis. In a logistic model, rhinoconjunctivitis yielded a 2-fold risk for current asthma with respect to rhinitis. Subjects with rhinoconjunctivitis had poorer quality of life (QoL); there was an impact on daily activities in 4.6% of rhinitis and 10.7% of rhinoconjunctivitis. Ocular symptoms increase the role of rhinitis as a risk factor for asthma and its impact on daily activities in children.
... About one billion people worldwide smoke (OMS-WHO, 2009). The most recent studies have tended to show an association between the development of atopic dermatitis in infants and passive exposure to tobacco smoke (Kramer et al., 2004;Bohme et al., 2010;Hansen et al., 2010), although some studies have reported inconclusive results (Ownby and McCullough, 1988;Strachan and Cook, 1998;Hjern et al., 2001;Hancox et al., 2008). ...
Article
Onset of atopic dermatitis and occurrence of related skin lesions are influenced by various environmental factors in humans, and companion animals. Several studies have demonstrated an association between passive smoking and the development of atopic dermatitis in children. This association has never been investigated in the dog to our knowledge. We enrolled 161 dogs seen at dermatology and vaccination consultations over a six-month period for this study. Dog owners were asked to complete a questionnaire, to evaluate the exposure of the dog to tobacco smoke. The atopic or non-atopic status of the dog was assessed on the basis of Favrot’s criteria (history, clinical examination and cutaneous cytology for Malassezia). Analysis of the data for the 161 dogs enrolled revealed a significant association between high levels of passive exposure to tobacco smoke (cigarette consumption divided by the area of the home) and the presence of atopic dermatitis in the dogs (OR, 4.38; 95% CI, 1.10–17.44; p = 0.03; NNH (number needed to harm) 3, 95% CI 2–52). The prevalence of atopic dermatitis showed a slight, but non-significant association with breed predisposition. Dogs with high levels of exposure to tobacco smoke may have a higher risk of atopic dermatitis than non-exposed dogs.
... The association between passive smoke exposure and childhood asthma is relatively well established8910. However, other studies have failed to demonstrate an association between smoking and asthma, and smokers were in some cases found to be at lower risk of developing asthma compared to nonsmokers or ex-smokers [11,12]. Studies in animal models confirm this dichotomy, and demonstrate that cigarette smoke (CS) can promote allergic sensitization and exacerbate allergic responses131415, but can also attenuate allergic inflammation and airway hyperresponsiveness during allergen challenge of previously sensitized animals16171819. ...
Article
Full-text available
Adverse health effects of tobacco smoke arise partly from its influence on innate and adaptive immune responses, leading to impaired innate immunity and host defense. The impact of smoking on allergic asthma remains unclear, with various reports demonstrating that cigarette smoke enhances asthma development but can also suppress allergic airway inflammation. Based on our previous findings that immunosuppressive effects of smoking may be largely attributed to one of its main reactive electrophiles, acrolein, we explored the impact of acrolein exposure in a mouse model of ovalbumin (OVA)-induced allergic asthma. C57BL/6 mice were sensitized to ovalbumin (OVA) by intraperitoneal injection with the adjuvant aluminum hydroxide on days 0 and 7, and challenged with aerosolized OVA on days 14--16. In some cases, mice were also exposed to 5 ppm acrolein vapor for 6 hrs/day on days 14--17. Lung tissues or brochoalveolar lavage fluids (BALF) were collected either 6 hrs after a single initial OVA challenge and/or acrolein exposure on day 14 or 48 hrs after the last OVA challenge, on day 18. Inflammatory cells and Th1/Th2 cytokine levels were measured in BALF, and lung tissue samples were collected for analysis of mucus and Th1/Th2 cytokine expression, determination of protein alkylation, cellular thiol status and transcription factor activity. Exposure to acrolein following OVA challenge of OVA-sensitized mice resulted in markedly attenuated allergic airway inflammation, demonstrated by decreased inflammatory cell infiltrates, mucus hyperplasia and Th2 cytokines. Acrolein exposure rapidly depleted lung tissue glutathione (GSH) levels, and induced activation of the Nrf2 pathway, indicated by accumulation of Nrf2, increased alkylation of Keap, and induction of Nrf2-target genes such as HO-1. Additionally, analysis of inflammatory signaling pathways showed suppressed activation of NF-kappaB, and marginally reduced activation of JNK in acrolein-exposed lungs, associated with increased carbonylation of RelA and JNK. Acrolein inhalation suppresses Th2-driven allergic inflammation in sensitized animals, due to direct protein alkylation resulting in activation of Nrf2 and anti-inflammatory gene expression, and inhibition of NF-kappaB or JNK signaling. Our findings help explain the paradoxical anti-inflammatory effects of cigarette smoke exposure in allergic airways disease.
... There are studies that show a direct association, 34 and conversely, a protective effect has also been reported. 35 In the current study, no association was found between passive smoking and the prevalence of asthma. ...
Article
Asthma is one of the most important diseases of childhood. The aim of this study was to evaluate the prevalence of asthma symptoms and risk factors affecting asthma. In a cross-sectional study design, 9991 children, aged 13-14 years in 61 primary schools in 32 districts of Istanbul were evaluated. Asthma prevalence among the children was assessed using the ISAAC protocol. In our study, a total of 10,894 questionnaires were distributed to 13-14 years old children, and of these 9991 questionnaires were suitable for analysis with an overall response rate of 91.7%. The rates of wheeze ever, wheezing in last 12 months and lifetime doctor diagnosed asthma prevalence were 17.4%, 9.0%, and 11.8%, respectively. There were 4746 boys (47.9%) and 5166 girls (52.1%) with M/F ratio of 0.92. Atopic family history, fewer than three siblings living at home, tonsillectomy or adenoidectomy history, consumption of fermented foods, mixed pickles, margarine and meat were found to be associated with an increased asthma risk. Use of paracetamol in the last 12 months, consumption of fruit and animal fats acted as a protective factor against asthma. The Mediterranean-style diet was not associated with the prevalence of asthma. Lifetime doctor diagnosed asthma prevalence was found to be 11.8% in 13-14 year olds. History of tonsillectomy and/or adenoidectomy and consumption of fermented foods, mixed pickles, margarine and meat may increase the symptoms of asthma. Usage of paracetamol and consumption of animal fats may be investigated as a protective factor against asthma.
... Some cross-sectional studies reported negative associations between passive smoking and respiratory symptoms in children [23][24][25] ; the authors suggested that tobacco exposure might also provide protective effects for childhood atopic diseases via selection mechanisms. However, in our study, children exposed to passive smoke had significantly higher risks for persistent cough, persistent phlegm, and wheezing, as in previous studies. ...
Article
Full-text available
Background Concentrations of ambient air pollution and pollutants in China have changed considerably during the last decade. However, few studies have evaluated the effects of current ambient air pollution on the health of kindergarten children. Methods We studied 6730 Chinese children (age, 3–7 years) from 50 kindergartens in 7 cities of Northeast China in 2009. Parents or guardians completed questionnaires that asked about the children’s histories of respiratory symptoms and risk factors. Three-year concentrations of particles with an aerodynamic diameter ≤10 µm (PM10), sulfur dioxide (SO2), and nitrogen dioxides (NO2) were calculated at monitoring stations in 25 study districts. A 2-stage regression approach was used in data analyses. Results The prevalence of respiratory symptoms was higher among children living near a busy road, those living near chimneys or a factory, those having a coal-burning device, those living with smokers, and those living in a home that had been recently renovated. Among girls, PM10 was associated with persistent cough (odds ratio [OR]PM10 = 1.44; 95% CI, 1.18–1.77), persistent phlegm (ORPM10 = 1.36; 95% CI, 1.02–1.81), and wheezing (ORPM10 = 1.31; 95% CI, 1.04–1.65). NO2 concentration was associated with increased prevalence of allergic rhinitis (OR = 1.96; 95% CI, 1.27–3.02) among girls. In contrast, associations of respiratory symptoms with concentrations of PM10, SO2, and NO2 were not statistically significant among boys. Conclusions Air pollution is particularly important in the development of respiratory morbidity among children. Girls may be more susceptible than boys to air pollution.
... Nicotine is an alkaloid in the tobacco plant Nicotiana tabacum, which has been considered as a useful drug in treatment of many diseases. Nicotine reduces the chance of preeclampsia [173] and atopic disorders such as allergic asthma [174]. Moreover, it has been shown to have a significant positive impact on neurodegenerative Parkinsonian symptoms, as it was reported by Fagerström et al. [175] as well as on patients with Alzheimer's disease [176]. ...
Article
Full-text available
To address the different types of pain (e.g. acute, chronic, neuropathic) different classes of medications, mainly non-steroidal anti-inflammatory drugs and narcotics (opioids), are used. More specifically, the alleviation or treatment of moderate to severe pain states commonly invokes the use of opioids. Unfortunately, their chronic administration induces various undesirable side effects, such as for example physical dependence and tolerance. One strategy to overcome these major side effects and to prolong the antinociceptive efficiency of the applied drugs involves the creation of multifunctional compounds which contain hybridized structures. Combination of opioid agonist and antagonist pharmacophores in a single chemical entity have been considered and extensively investigated, but opioids have also been combined with other bioactive neurotransmitters and peptide hormones that are involved in pain perception (e.g. substance P, neurotensin, cholecystokinin, cannabinoids, melanocortin ligands, etc.). Such novel chimeras (also called designed multiple ligands or twin/triplet drugs), may interact independently with its respective receptors and potentially results in more effective antinociceptive properties. The designed multiple ligands presented in this work include opioid-non-opioid peptide dimer analogues, mixed peptidic-non-peptidic bifunctional ligands and dual non-peptidic dimers. The main focus herein is placed on the design and biological evaluation of these multiple opioid compounds, rather than the synthetic approach and preparation.
... There are indications that other non-allergenic agents also have an inhibitory effect on the atopic status. A negative correlation for instance between personal or parental smoking and atopy was described202122. Sunyer et al. (1997) found a positive association between smoking and bronchial hyperresponsiveness in non-atopics and a lack of the association in atopics. ...
Article
Full-text available
Background We have investigated the relationship between atopic status and long-term occupational exposure to latex proteins or methyl diethyl diisocyanate (MDI) as high and low molecular weight asthma-inducing agents, respectively. Methods This study is based on retrospective analyses of two groups of symptomatic outpatients: 184 healthcare workers with latex exposure and 156 workers with isocyanate (MDI) exposure. We analysed atopic and non-atopic subgroups according to exposure duration and the frequencies of specific sensitization. Results 45% of the healthcare subgroup specifically sensitized to latex were atopic, whereas in the non-sensitized healthcare subgroup only 26% were atopic. On the other hand, subjects specifically sensitized to MDI were rarely atopic (only 15%), whereas in the subgroup non-sensitized to MDI atopy was present in 38%. After prolonged durations of exposure, the proportion of atopics was further elevated in most healthcare subgroups but it decreased in the MDI-exposed subjects. Conclusions We hypothesize that latex proteins as sensitizing agents might promote the development of atopy, whereas exposure to the low molecular weight MDI might inhibit the atopic status.
... It has been observed that the children who are exposed in utero have a greater risk of presenting wheezing at some time during their lives and in the previous year [32]; in the same way, they also have a greater necessity of medical attention for asthma in the emergency services [33]. When considering the passive exposure to and the prevalence of, asthma, the results have been contradictory, discovering studies with a direct association [9,33], and others in which, inclusively, a protective effect has been reported [34]. Finally, active smoking appears not to be associated with either asthma or with its symptoms [9]. ...
Article
Full-text available
Asthma has increased in various regions of the world. The factors associated with the growth in prevalence are still to be determined. To evaluate the degree of association of the prevalence of asthma with passive smoking and obesity in school-children in western Mexico. A population-based cross-section analytic study. A stratified random sample of 740 primary school pupils of between 6 and 12 years of age was chosen. Asthma, passive smoking and a background of allergic diseases were identified by means of a standardized questionnaire filled out by the parents of the participants. Obesity was identified by means of the body mass index. Proportional sections of population were estimated and the degree of association between asthma (dependent variable) and the independent variables was evaluated by means of multivariate logistic regression. THE FOLLOWING FACTORS OF PREVALENCE WERE FOUND: asthma 8.1%; obesity 19.9%; background of smoking in the father 6.7% and in the mother 13.3%. There was no significant association to be found with asthma in either passive smoking where one of the parents smoked (p = 0.39) or in obesity (p = 0.09). On the other hand, the background of allergic diseases in the mother showed statistically significant association with asthma in the boys (odds ratio = 3.5, 95% confidence interval 1.4 to 8.59), but not in the girls. With the exception of the maternal background of allergy, neither obesity nor passive smoking are factors associated with asthma in Mexican children.
... One study reported a reduced risk of rhinoconjunctivitis for adult smokers and their children. 17 Another showed a decreased risk of hayfever in adolescents who were exposed to tobacco in utero. 18 However, in the ISAAC Phase Two Study there was an increased risk of rhinoconjunctivitis in children aged 9e11 years who had been exposed to maternal smoking during pregnancy. ...
Article
Full-text available
Exposure to parental smoking is associated with wheeze in early childhood, but in 2006 the US Surgeon General stated that the evidence is insufficient to infer a causal relationship between exposure and asthma in childhood and adolescents. To examine the association between maternal and paternal smoking and symptoms of asthma, eczema and rhinoconjunctivitis. Parents or guardians of children aged 6-7 years completed written questionnaires about symptoms of asthma, rhinoconjunctivitis and eczema, and several risk factors, including maternal smoking in the child's first year of life, current maternal smoking (and amount) and paternal smoking. Adolescents aged 13-14 years self completed the questionnaires on these symptoms and whether their parents currently smoked. In the 6-7-year age group there were 220 407 children from 75 centres in 32 countries. In the 13-14-year age group there were 350 654 adolescents from 118 centres in 53 countries. Maternal and paternal smoking was associated with an increased risk of symptoms of asthma, eczema and rhinoconjunctivitis in both age groups, although the magnitude of the OR is higher for symptoms of asthma than the other outcomes. Maternal smoking is associated with higher ORs than paternal smoking. For asthma symptoms there is a clear dose relationship (1-9 cigarettes/day, OR 1.27; 10-19 cigarettes/day, OR 1.35; and 20+ cigarettes/day, OR 1.56). When maternal smoking in the child's first year of life and current maternal smoking are considered, the main effect is due to maternal smoking in the child's first year of life. There was no interaction between maternal and paternal smoking. This study has confirmed the importance of maternal smoking, and the separate and additional effect of paternal smoking. The presence of a dose-response effect relationship with asthma symptoms suggests that the relationship is causal, however for eczema and rhinoconjunctivitis causality is less certain.
... Cigarette smoke exposure results in more frequent asthma attacks and symptoms, impairment in lung function and decreased efficacy of short-term inhaled corticosteroid treatment in steroid-naïve patients with asthma (Althius et al., 1999; James et al., 2004; Siroux et al., 2000). Although some clinical trials suggest that smokers have a lower risk of developing asthma symptoms when compared with nonsmokers and ex-smokers (Hjern et al., 2001; McWhorter et al., 1989; Tsoumakidou et al., 2007), such findings should be interpreted ...
Article
We evaluated the effects of cigarette smoke (CS) on lung inflammation and remodeling in a model of ovalbumin (OVA)-sensitized and OVA-challenged mice. Male BALB/c mice were divided into 4 groups: non-sensitized and air-exposed (control); non-sensitized and exposed to cigarette smoke (CS), sensitized and air-exposed (OVA) (50 μg+OVA 1% 3 times/week for 3 weeks) and sensitized and cigarette smoke exposed mice (OVA+CS). IgE levels were not affected by CS exposure. The increases in total bronchoalveolar fluid cells in the OVA group were attenuated by co-exposure to CS, as were the changes in IL-4, IL-5, and eotaxin levels as well as tissue elastance (p<0.05). In contrast, only the OVA+CS group showed a significant increase in the protein expression of IFN-γ, VEGF, GM-CSF and collagen fiber content (p<0.05). In our study, exposure to cigarette smoke in OVA-challenged mice resulted in an attenuation of pulmonary inflammation but led to an increase in pulmonary remodeling and resulted in the dissociation of airway inflammation from lung remodeling.
... this must be examined further (Kramer et al., 2004;Seymour et al., 1997). With regard to the development of AD in children, exposure to maternal smoking in utero and/or exposure to smoke in the first year after birth might be more detrimental than paternal smoking (Hjern et al., 2001). Fetal exposure to tobacco smoke products in the amniotic fluid can have long-term effects on gut immune responses and could be important in allergic sensitization (Gilliland et al., 2002). ...
Article
A systematic review was conducted to examine epidemiological and other medical findings regarding 8 clinical questions to investigate associations between passive smoking and allergic diseases in childhood. Passive smoking was associated with the following in childhood: increased risk of onset, aggravation, and impaired respiratory function in asthma; increases in coughing and sputum. Maternal smoking during pregnancy was associated with onset of asthma in childhood, and persistent impairment of respiratory function from birth. Passive smoking was suggested as a risk factor associated with onset and aggravation of allergic rhinitis, and was also associated with increases in total IgE levels and positive specific IgE test and skin prick test results. In particular, passive smoking during early infancy was significantly associated with sensitization to food and indoor allergens. Reported studies on atopic dermatitis and food allergies were limited, and findings on their associations with passive smoking were contradictory. Thus, their causal relationship was inconclusive in this study. In sum, passive smoking has serious impacts on allergic diseases in childhood and proactive avoidance of passive smoking is recommended.
Article
Atopic eczema (AE), or atopic dermatitis (AD), is a common inflammatory skin disease with a disrupted epidermal barrier and an allergic immune response. AD/AE is prominently characterized by a symptomatic itch and transient skin lesions. Infants compose a significant percentage affected. Two models have been proposed to explain AD/AE skin pathology: the gut microbiome-focused inside-outside model and the outside-inside model concentrating on the disrupted skin barrier/skin microbiome. Gene disruptions contributing to epidermal structure, as well as those in immune system genes, are implicated. Over 30 genes have been linked to AD/AE with Flg and Tmem79/Matt alterations being common. Other linked disruptions are in the interleukin-1 family of cytokines/receptors and the TH2 gene family of cytokines. Inheritable epigenetic modifications of the genes or associated proteins may also be involved. Skin barrier disruption and the allergic immune response have been the main foci in mechanistic studies of AD/AE, but the role of the environment is becoming more apparent. Thus, an examination of in utero exposures could be very helpful in understanding the heterogeneity of AD/AE. Although research is limited, there is evidence that developmental exposure to environmental tobacco smoke or phthalates may impact disease. Management for AD/AE includes topical corticosteroids and calcineurin inhibitors, which safely facilitate improvements in select individuals. Disease heterogeneity warrants continued research not only into elucidating disease mechanism(s), via identification of contributing genetic alterations, but also research to understand how/when these genetic alterations occur. This may lead to the cure that those affected by AD/AE eagerly await.
Article
BACKGROUND: Atopic dermatitis (eczema) in childhood is socially patterned, with higher incidence in more advantaged populations. However, it is unclear what factors explain the social differences. OBJECTIVES: To identify early-life risk factors for eczema, and to explore how early-life risk factors explain any differences in eczema. METHODS: We estimated odds ratios (ORs) for ever having had eczema by age 5 years in 14 499 children from the U.K. Millennium Cohort Study (MCS), with a focus on maternal, antenatal and early-life risk factors and socioeconomic circumstances (SECs). Risk factors were explored to assess whether they attenuated associations between SECs and eczema. RESULTS: Overall 35.1% of children had ever had eczema by age 5 years. Children of mothers with degree-level qualifications vs. no educational qualifications were more likely to have eczema (OR 1.52, 95% confidence interval 1.31-1.76), and there was a gradient across the socioeconomic spectrum. Maternal atopy, breastfeeding (1-6 weeks and >/= 6 months), introduction of solids under 4 months or cow's milk under 9 months, antibiotic exposure in the first year of life and grime exposure were associated with an increased odds of having eczema. Female sex, Pakistani and Bangladeshi ethnicity, smoking during pregnancy, exposure to environmental tobacco smoke and having more siblings were associated with reduced odds for eczema. Controlling for maternal, antenatal and early-life characteristics (particularly maternal smoking during pregnancy, breastfeeding and number of siblings) reduced the OR for eczema to 1.26 (95% confidence interval 1.03-1.50) in the group with the highest educational qualifications compared with the least. CONCLUSIONS: In a representative U.K. child cohort, eczema was more common in more advantaged children. This was explained partially by early-life factors including not smoking during pregnancy, breastfeeding and having fewer siblings.
Article
Background. In the place there are chemical, petrochemical and granaries companies. There are registrered 130.000 vehicles. Studies were realized on prevalence of diseases and factors of risk in different zones. There is not known the prevalence of respiratory diseases in the city. Proposes. To describe the frequency of asthma, rinitis and factors of risk. To carry out comparisons. Methodology. Study of transverse cut for modality of survey of multiple proposes in homes. For the estimation of n there was in use the prevalence of asthma (4%), found in previous studies, a mean error of 0.8% (ER = 20%) and a confidence level of 95%. A sampling was effected by conglomerates with subsampling, by proportional probabilities to its size, applying the effect of design (deff=2). The questionnaire applyed was used in other studies. Results. There were polled 1447 housings, n = 4766 persons. The 18% answered to suffer some kind of respiratory disease. Rhinitis: 12.7% (607/4766), Symptoms Indicators of Asthma (SIA): 3.4% (163/4766) and asthma: 2.6% (125/4766). The 19.8% was suffering SIA with rhinitis -OR = 3.57 (95% CI: 2.30-5.54)- and 17.8% of those who were recounting asthma they were suffering rhinitis -OR = 3.04 (95% CI: 1.83-5.07)-. The prevalence of smoking was 20%, being association between inhaling smoke and SIA. Association was situated among obesity and rhinitis. Conclusions. The prevalence of asthma and rhinitis was similar to found in Argentina. SIA's frequency was glaringly low. The prevalence of asthma in the city would be 6%. There is corroborated the made subdiagnosis of asthma that its ratified to the inadequate above-mentioned treatments. The comparison with the results of the previous studies, they will corroborated or not the existence of areas of major risk to suffer respiratory disease.
Article
Thymic stromal lymphopoietin (TSLP) is regarded as the main factor responsible for the pathogenesis of atopic dermatitis (AD). Cigarette smoke is an aggravating factor for allergies, but has been reported to decrease the risk of AD. In the present study, we evaluated the role of nicotine, the main constituent in cigarette smoke extract, and its underlying mechanism of action in the regulation of TSLP expression. We found that nicotine significantly inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced TSLP expression in BALB/c mice and the mouse keratinocyte cell line PAM212. Nicotine inhibition of TSLP production was abolished by pretreatments with α7 nicotinic acetylcholine receptor (α7 nAChR) antagonists, AMP-activated protein kinase (AMPK) inhibitor, and phosphoinositide 3-kinase (PI3K) inhibitors. The same inhibitors abolished inhibition of nuclear factor-κB (NF-κB) activation by nicotine. These results suggest that nicotine inhibits the expression of TSLP by suppressing the activation of NF-κB through the α7 nAChR-PI3K-AMPK signaling pathway.
Article
A HPTLC method for the quantitative analysis of nicotine present in the various commercial tobacco preparations has been developed. Methanol extract of the formulations were analyzed on a silica gel 60 GF254 TLC plates with spot visualization under UV and scanning at 235 nm in absorption-reflection mode. Calibration curves were found to be linear in the range 2μg-25 μg. The Correlation coefficients were found to be 0.991 for nicotine. The average recovery rate was 95% (CV% 1.35) for nicotine. From the present study LOD was determined as 0.08 μg/spot for Nicotine. The validity of the method with respect to analysis was confirmed by comparing the UV spectra of the commercial tobacco preparation with that of the standard within the same Rf window.
Article
Background: Patients with asthma who smoke have reduced lung function, increased exacerbation rates and increased steroid resistance compared to non-smoking asthmatics. In mice, cigarette smoke has been reported to have both pro- and anti-Th2 response effects. Objective: We hypothesized that combining tobacco cigarette smoke (tCS) with allergen exposure increases inflammation, airway remodeling and lung function in mice. To test this hypothesis we combined a severe triple allergen model with tCS-exposure and investigated if effects were due to Toll like receptor 4 signalling and/or nicotine and also observed when nicotine-free cigarettes were used. Methods: Mice were sensitized with ovalbumin, cockroach and house dust mite allergen in alum followed by intratracheal challenges with allergen twice a week for six weeks or additionally exposed to tCS during the allergen challenge period. Nicotine or nicotine-free herbal cigarette smoke was also applied to allergen challenged mice. Results: tCS significantly reduced eosinophil numbers, IL-4 and IL-5 concentrations in the lung, total and allergen-specific IgE in serum, improved lung function and reduced collagen I levels. With the exception of collagen I all parameters reduced by tobacco cigarette smoke were also reduced in Toll like receptor 4 deficient mice. Nicotine-free cigarette smoke also had significant anti-inflammatory effects on eosinophil, IL-4 and IL-5 concentrations in the lung and reduced airway hyperreactivity, albeit weaker than tobacco smoke. Applying nicotine alone also reduced Th2 cytokine levels and eosinophil numbers in the airways. Conclusion: Our experiments show that tCS-exposure reduces allergen-induced Th2 response in the lung and associated collagen I production and development of airway hyperreactivity. With the exception on collagen I formation, these effects were not dependent on Toll like receptor 4. The observed anti-Th2 effects of both nicotine and nicotine-free herbal cigarette smoke together suggests that tCS reduces the Th2 responses through nicotine and other products released by burning tobacco. This article is protected by copyright. All rights reserved.
Article
Full-text available
Emerging evidence suggests that integrity of blood-brain barrier is pivotal to pathology and pathogenesis of vascular-based neurodegenerative disorders. We have recently reported blood-brain barrier protective effects of nutraceutical agents with anti-inflammatory properties in an established dietary-induced BBB dysfunction model. Studies also reported that nicotine exhibits anti-oxidative/-inflammatory effects and improve cognitive impairment in Alzheimer's disease. However there has been no studies reporting the effect of nicotine on high-fat-induced BBB dysfunction. In the present study, we investigated the effect of nicotine on BBB integrity and neuro-inflammation in an established mouse model of BBB disruption induced by a diet enriched in saturated fatty acids (SFA). Wild-type C57BL/6J mice were fed chow enriched in SFA (23% w/w) with/without nicotine for 10 weeks. Compared to mice maintained on SFA-free and low-fat (LF) chow (4% w/w), capillary permeability indicated by the parenchymal extravasation of plasma derived IgG, was significantly greater in the SFA treatment group. Nicotine provided concomitantly with the SFA diet significantly attenuated IgG extravasation, however it remained significantly greater than LF-controls. Markers of neurovascular inflammation GFAP, COX-2 and GRP78 remained exaggerated in SFA+nicotine treated mice compared to LF-controls. Nicotine did however modestly, but not significantly, improve plasma total anti-oxidative status in SFA fed mice. Nicotine moderately attenuated BBB disruption induced by chronic ingestion of high-SFA diet, but had no significant effect on neuroinflammation per se. © The Author 2015. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
Article
Ischemic injury in rodent models reliably leads to the activation of microglia, which might play a detrimental role in neuronal survival. Our preliminary studies suggest that nicotine plays a potential role in decreasing the numbers of cultured microglia in vitro. In the present study, we found treatment with nicotine 2, 6, and 12 h after ischemia for 7 days significantly increased the survival of CA1 pyramidal neurons in ischemia/reperfusion rats. This effect was accompanied by a significant reduction in the increase of microglia rather than astrocytes, as well as a significant reduction of enhanced expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) in CA1 induced by ischemia/reperfusion. Nicotine inhibits microglial proliferation in primary cultures with and without the stimulation of granulocyte-macrophage colony-stimulating factor (GM-CSF). Pre-treatment with α-bungarotoxin, a selective α7 nicotinic acetylcholine receptor (α7 nAChR) antagonist, could prevent the inhibitory effects of nicotine on cultured microglial proliferation suggesting that nicotine inhibits the microglial proliferation in an α7 nAChR-dependent fashion. Our results suggest that nicotine inhibits the inflammation mediated by microglia via α7 nAChR and is neuroprotective against ischemic stroke, even when administered 12 h after the insult. α7 nAChR agonists may have uses as anti-ischemic compounds in humans.
Article
A recent study hypothesized that a skin-mediated immune response leads to atopic sensitization. However, prospective studies investigating sensitization during infancy are limited. This cohort study included unselected infants born at NTT Medical Center Tokyo between March 2008 and February 2009. At age 3, 6, 9, and 12 months, they underwent physical examinations and a skin prick test (SPT). Associations of predictor variables with sensitization, atopic dermatitis (AD), and food allergy (FA) at ≤1 year were analyzed. Of 317 infants, the SPT was positive in 25 (8%) at 3 months and 133 (42%) at least once. Of the SPT-positive infants at 3 months, 19 (76%) had atopic diseases at ≤1 year (OR, 13.9; 95% 95%CI, 5.3-36.6). The presence of dermatitis at ≤3 months was significantly associated with sensitization (aOR, 3.0; 95%CI, 1.8-5.0), AD (aOR, 13.0; 95%CI, 4.5-37.3), and FA (aOR, 28.4; 95%CI, 3.3-240.6) by the age of 1 year. Point prevalence of sensitization paralleled the incidence of dermatitis. Almost all FA infants had experienced dermatitis at ≤3 months. In infants with dermatitis at ≤3 months, breast-feeding was significantly associated with sensitization (OR, 2.5; p=0.005) and FA (OR, 3.0; p=0.004). Infants without eczema at ≤3 months rarely developed AD or FA. The presence of dermatitis in the first few months after birth is a strong risk factor for atopic sensitization and FA during the first year of life.
Article
Environmental tobacco smoke and constituents are global risks for human health. Considerable evidence shows that environmental tobacco smoke exposure contributes to, and exacerbates, respiratory disorders. This review assesses the causal role of environmental tobacco smoke exposure for childhood respiratory disorders, and in particular asthma. Tobacco smoke and environmental tobacco smoke exposure during pregnancy have an effect upon lung function in newborn infants; exposure after birth also has an effect upon lung function. An effect upon bronchial responsiveness has been suggested but the evidence is not as strong as for lung function. From 1997 to 1999 a comprehensive set of systematic reviews concerning the relationship between exposure to environmental tobacco smoke and respiratory health in children summarized the results from hundreds of published papers. The evidence for a causal relationship between environmental tobacco smoke exposure and asthmatic symptoms on the one hand, and between environmental tobacco smoke exposure and reduction in lung function on the other hand, was quite strong, whereas the evidence between environmental tobacco smoke exposure and development of allergy was much weaker. Here we present an overview of the effects of environmental tobacco smoke exposure on lung health in children. A hypothesis has been put forward regarding upregulation of pulmonary neuroendocrine cells in relationship to mechanisms of tobacco smoke products (TSP)-induced pulmonary disease. It has also been reported that genetic variation makes part of the population especially vulnerable to environmental tobacco smoke exposure during pregnancy. Furthermore, there is a need for intervention to reduce environmental tobacco smoke exposure in young children, by educating parents and adolescents about the health effects of environmental tobacco smoke exposure. Studies are needed to identify possible critical periods when environmental tobacco smoke exposure is more likely to induce harmful effects on lung health in young children in order to implement effective preventive strategies.
Article
Full-text available
Tobacco is implicated in multisystemic carcinogenesis through more than fifty identified carcinogenic metabolites that produce mutations responsible for alterations in cell cycle, immune response and endocrine regulation. Is one of nine risk factors identified in one third of cancer deaths together with obesity, sedentary, alcohol consumption, sexual promiscuity, drug addiction, and open and closed air contamination. Answering for cardiovascular diseases as the first cause of death in civilized world, tobacco is also pointed as the major factor implicated in the development of COPD (chronic obstructive pulmonary disease), RB-ILD (respiratory bronchiolitis and interstitial lung disease), DIP (desquamative interstitial pneumonia), bronchiolitis and bronchiolocentric interstitial fibrosis, Langerhans cells histiocytosis, eosinophilic pneumonia, sarcoidosis, epidermoid metaplasia in respiratory epithelium and lung cancer. The chronic tobacco induced inflammatory state is the basis for the acquisition of genetic alterations dependent on the tobacco contaminants.
Article
Our previous studies showed that Aflatoxin G1 (AFG1) could induce lung adenocarcinoma, and that the cancer cells originated from alveolar type II cells (AT-II cells). Recently, we found AFG1 induced structural impairment in rat AT-II cells, which may account for an early event in lung tumorigenesis. However, the mechanism of AFG1-induced AT-II cell damage remains unclear. DNA damage and apoptosis induced by oxidative stress are well accepted causes of cell damage. Thus, we explore whether AFG1 activates the reactive oxygen species (ROS)/MAPK/apoptosis pathway to cause cell damage in human AT-II cells like the cell line (A549). We found AFG1 induced oxidative stress by increasing ROS generation and caused DNA double-strand breaks (DSBs) by up-regulating γH2AX expression. AFG1 also triggered apoptosis in A549 cells by regulating Fas/FasL, caspase-8, Bax, Bcl-2, and activating caspase-3. Pre-treatment with antioxidant N-acetyl- L-cysteine (NAC) reduced ROS generation and DNA DSBs, inhibited apoptosis, and increased cell viability in AFG1-treated cells. Furthermore, we found AFG1 activated ROS-mediated JNK and p38 pathways to induce cell apoptosis in A549 cells. In conclusion, our results indicate that AFG1 induces oxidative DNA damage and triggers apoptosis through ROS-mediated JNK and p38 signaling pathways in A549 cells, which may contribute to AFG1-induced AT-II cell damage.
Article
Aim: To assess the associations between nutrition supplements in infancy and later asthma and allergy in school-age children, and to explore the impact of environmental factors in early life. Methods: Five hundred and two children underwent clinical examination, skin prick test and a second parentally completed questionnaire within 2 y of a cross-sectional questionnaire-based study, including 4585 primary school children (6–16 y old) in 1994 from urban Oslo (37%), the mountainous area of Hallingdal (42%), and the industrial, coastal area of Odda (21%). The children were selected from the 1994 survey on the basis of reported diagnosed asthma (n=166), wheeze in the last 12 mo (n=155) and no asthma/no wheeze (n=181). Questions were related to nutrition and environmental exposure in early life. Possible associations between allergic sensitization or asthma at school age and exposures were estimated by logistic regression analysis, adjusting for potential confounders. Results: Daily intake of fresh fruit or vegetables, but not extra vitamins or cod liver oil supplements, in infancy decreased the risk of asthma (adjusted odds ratio (aOR) 0.57 (95% confidence interval (CI): 0.37–0.88). Early supplements of cod liver oil and extra vitamins were associated with increased allergic sensitization (aOR 1.78 (95% CI: 1.03–3.07) and 1.71 (95% CI: 1.01–2.88), respectively). A significantly higher prevalence of allergic sensitization was found in children living in Hallingdal compared to Odda, while the latter children, on the other hand, had the highest prevalence of house dust mite allergy ( p=0.001 vs Hallingdal and p=0.04 vs Oslo).
Article
Asthma, hay fever and eczema became a public health problem following a marked increase in the prevalence of these conditions in the second half of the 20th century. However, the rise in the incidence of allergies and asthma now appears to have halted, at least in children. Before puberty, asthma and hay fever occur most frequently in boys. However, this ratio is reversed after puberty. Allergic diseases, especially hay fever, were mainly an upper-class disease in the 1800s. However this is no longer the case; today, asthma is a more common condition, and its symptoms are most severe, in lower-income social groups. An important reason for this is that smoking is now more widespread in these groups. The origins of this rise in the prevalence of asthma and allergies are still unclear, but they seem to be linked to changing contact with microbes1, mainly bacteria and parasites, in early life. Various cost factors can also be significant. It is important to distinguish between factors that contribute to the pathogenesis of the condition and those that exacerbate allergic reactions. Air pollutants, pollen and animal hair contribute to an increase of symptoms in people with asthma and allergies but seldom lead to the development of these diseases in people who are healthy. The socioeconomic costs of air pollutants, for example, can nonetheless be significant since a large proportion of the population is exposed to them and asthma and allergies are common in the population. Additional factors such as tobacco smoke can contribute to the onset of asthma in healthy people and to the aggravation of allergic problems in sufferers.
Article
A high-pressure thin-layer chromatography (HPTLC) method for quantitative analysis of nicotine in Nicotiana sp. was developed using a methanol extract of leaves and stems and TLC plates (silica gel 60 GF254) with spot visualization under ultraviolet (UV) light. Scanning at 235 nm in the absorption-reflection mode produced linear calibration curves in the range of 2 to 25 μg, with a correlation coefficient of 0.991. The average recovery rate was 95% (CV % 1.35). From the present study, the lower limit of detection was 0.08 μg spot−1 for the nicotine. The validity of the method was confirmed by comparing the UV spectra of the tobacco plant samples with standards within the same Rf window.
Article
Consumption of tobacco is hazardous to the health. It leads to cardiovascular diseases, and increases the incidence of numerous neoplasms. The adverse effects on the skin are less well-known and often ignored. Changes in the rheologic characteristics of the blood, increased vasoconstriction and damage to the epithelial layer of the vessel play an important pathogenic role in impaired wound healing, thromboangiitis obliterans and peripheral arterial obstructive diseases. Interactions with collagen metabolism are of special significance in wound healing and skin aging. The immunological effects, such as the induction of an inflammation reaction play a role in palmoplantar pustulosis, psoriasis, atopic dermatitis, acne vulgaris, acne inversa, thromboangiitis obliterans and lupus erythematodes. In addition, immunosuppression caused by nicotine consumption may contribute to the pathogenesis of human papilloma-virus infections, malignant melanoma and epithelial tumors of the skin and neighboring mucous membranes.
Chapter
Many studies have shown the detrimental role of smoking on development and progression of pulmonary diseases such as chronic bronchitis, COPD, asthma, lung cancer, and some interstitial lung diseases. The role of oxidative stress is in this respect is variable, clearly established in COPD, and either less explicitly present or not reported because lack of studies in the other diseases.
Article
Zusammenfassung: In den letzten Jahrzehnten wird ein deutlicher Anstieg allergischer Erkrankungen wie Asthma, Heuschnupfen und atopische Dermatitis beobachtet. Epidemiologische Studien zeigten, daß dieser Anstieg nicht durch geänderte Diagnosedefinitionen zustande kommt. Eine komplexe Interaktion zwischen genetischen Faktoren und Umwelteinflüssen ist für dieses Phänomen verantwortlich. Genetisch prädisponierte Menschen haben eine erhöhte Empfindlichkeit, Asthma oder andere allergische Erkrankungen zu entwickeln, wenn sie bestimmten Umwelt- und Lebensstileinflüssen ausgesetzt sind. Passivrauchen erhöht laut zahlreicher Studien das Risiko für Asthma, und einige zeigen auch ein erhöhtes Risiko für Atopie. Diese Assoziation ist für die Exposition gegenüber Schwefeldioxid, Staub, Dieselruß und Ozon weniger klar. Lebensstilfaktoren wie sozioökonomischer Status, Geschwisterzahl, Infekte im frühen Kindesalter, Eßgewohnheiten, Aufwachsen in einer anthroposophisch orientierten Familie oder auf einem Bauernhof, scheinen große Relevanz für die Entwicklung allergischer Erkrankungen zu haben. Derzeit herrscht große Unsicherheit darüber, welche Empfehlungen als Primärprävention gegeben werden sollen. Rezente Studien haben alte Paradigmen in Frage gestellt, wonach Vermeiden von frühem Allergenkontakt der Entwicklung allergischer Erkrankungen vorbeugen würde. Konsens besteht darüber, daß Rauchen während der Schwangerschaft und kindliches Passivrauchen als Primärprävention vermieden werden sollen.
Article
Cigarette smoking is a major risk to the overall burden of disease in developed countries. Smoking influences disease development, disease outcome and therapeutic success. Cigarettes with low tar, which do less harm, do not exist, nor there is a safe level of smoking. Passive smoking is involuntary inhalation of tobacco smoke. Environmental tobacco smoke is the second most common cause of carcinogen exposure. Passive smoking, whether prenatal or postnatal in children, increases the likelihood of asthma, similar as in adults. Active smoking increases total immunoglobulin E (IgE) level and inflammatory cell infiltration, especially eosinophils. Tobacco smoking increases bronchial hyperreactivity. Clinical picture of asthma in smokers is more severe in terms of symptoms, with more frequent exacerbations and invasive intubation with increased mortality rate than in asthmatics nonsmokers. Smokers have a higher prevalence of allergic rhinitis and atopic dermatitis.
Article
Background: Allergic rhinitis affects a significant proportion of the European population. Few surveys have investigated this disorder in Greek adults. Our objective was to describe the characteristics of patients with allergic rhinitis in an adult outpatient clinic in Thessaloniki, Greece. Methods: We studied the medical records of adult patients referred to a Clinical Immunology outpatient clinic from 2001 to 2007. The diagnostic procedure was not changed during the whole study period, including the same questionnaire used at the time of diagnosis, skin prick tests, and serum specific IgE. Results: A total of 1851 patient files with diagnosed allergies were analysed and allergic rhinitis was confirmed in 711 subjects (38.4%). According to ARIA classification, persistent allergic rhinitis was more prevalent than intermittent (54.9% vs. 45.1%), while 60.8% of subjects suffered from moderate/severe disease. In multivariable analysis, factors associated with allergic rhinitis were age (for every 10 years increase, OR: 0.84, 95% CI: 0.77-0.91; p<0.001); working in school environment (teachers or students) (OR: 1.46, 95% CI: 1.05-2.02; p=0.023); parental history of respiratory allergy (OR: 2.41, 95% CI: 1.69-3.43; p<0.001); smoking (OR: 0.71, 95% CI: 0.55-0.91; p=0.007); presence of allergic conjunctivitis (OR: 6.16, 95% CI: 4.71-8.06; p<0.001); and asthma (OR: 2.17, 95% CI: 1.57-3.01; p<0.001). Analysis after multiple imputation corroborated the complete case analysis results. Conclusions: Allergic rhinitis was documented in 38.4% of studied patients and was frequently characterised by significant morbidity. Factors associated with allergic rhinitis provide insight into the epidemiology of this disorder in our region. Further studies on the general population would contribute to evaluating allergic rhinitis more comprehensively.
Article
Full-text available
The objective of this study was to assess the role of parental smoking in changes, after a four year interval (1983-7), in the prevalence and severity of the atopic state in 166 pre-adolescent children. Allergy skin prick tests were related to parental smoking habits and their changes during this same interval. The total number of cigarettes smoked by parents decreased in 56 families while it increased in only 16. Boys had significantly more persistently positive skin tests and changed more frequently from negative to positive. The skin test index did not show significant changes in girls. This index did not change in children of persistent non-smokers or those starting to smoke during this period, while it increased among sons of those that quit smoking and of persistent smokers. This was not only due to those boys who became skin test positive during follow up. When analysis was restricted to 14 boys who had been skin test positive in 1983 and whose parents were persistent smokers, the index increased in eight, remained unchanged in four, and decreased in only two. This report supports the hypothesis that parental smoking is a factor that, together with specific allergenic exposure, may enhance allergic sensitisation in children.
Article
Full-text available
To test the hypothesis that smoking increases the risk of sensitisation by occupational allergens. Historical prospective cohort study. Platinum refinery. 91 Workers (86 men) who started work between 1 January 1973 and 31 December 1974 and whose smoking habit and atopic state (on skin prick testing with common allergens) had been noted at joining. Results of skin prick tests with platinum salts carried out routinely every three to six months and records of any respiratory symptoms noted by the refinery's occupational health service. Follow up was until 1980 or until leaving refinery work, whichever was earlier. 57 Workers smoked and 29 were atopic; 22 developed a positive result on skin testing with platinum salts and 49 developed symptoms, including all 22 whose skin test result was positive. Smoking was the only significant predictor of a positive result on skin testing with platinum salts and its effect was greater than that of atopy; the estimated relative risks (95% confidence interval) when both were included in the regression model were: smokers versus non-smokers 5.05 (1.68 to 15.2) and atopic versus non-atopic 2.29 (0.88 to 5.99). Number of cigarettes smoked per day was the only significant predictor of respiratory symptoms. Smokers are at increased risk of sensitisation by platinum salts.
Article
Full-text available
Recent studies have indicated that atopic sensitisation is uncommon while respiratory symptoms are common among schoolchildren in Eastern Europe. Risk factors for respiratory symptoms and atopic sensitisation were evaluated in a cross sectional study involving 2594 schoolchildren (10-12 years) from Sweden (n = 665), Poland (n = 410), and Estonia (n = 1519). The measurements included parental questionnaires and skin prick tests with eight standardised allergens. Multiple logistic analyses demonstrated that atopic heredity was a significant independent risk factor for respiratory symptoms and atopic sensitisation in all the countries. Current dampness and maternal smoking were related to respiratory symptoms whereas domestic crowding, male gender, and passive smoking during infancy were related to atopic sensitisation. Current maternal smoking had a strong dose response association with current coughing attacks (nocturnal cough > 4 weeks or exercise induced coughing attacks) but only in Eastern Europe. A strong inverse relationship was recorded between domestic crowding and sensitisation as the risk for sensitisation increased with decreasing number of persons per room in the household (odds ratio (OR) 0.58, 95% confidence interval (CI) 0.43 to 0.77). Exposure to tobacco smoke at home during infancy was a risk factor for atopic sensitisation but only to animal dander and only in Eastern Europe (OR 1.41, 95% CI 1.03 to 1.93). In conclusion, there were small differences in the pattern of risk factors between Eastern and Western Europe. The only exception was environmental tobacco smoke being a risk factor only in Eastern Europe. The study also suggests that factors related to domestic crowding protect against atopic sensitisation in Estonia and Poland. A higher standard of living with less crowding may give rise to an increasing prevalence of atopic sensitisation also in Eastern Europe.
Article
Full-text available
We have compared the prevalence of asthma, bronchial hyperresponsiveness (BHR), and atopy in relation to parental smoking in children aged 7 to 13 years. Information on the presence of asthma was obtained from a questionnaire, BHR was assessed by a methacholine challenge test, and atopy was defined as a positive response to a skin prick test. A complete history of the parents' smoking habits during their children's life, including prenatal smoking habits, was recorded. The prevalence of maternal smoking increased from 37.9% during pregnancy to 45.3% at the cross-sectional survey. None of the outcomes was significantly related to paternal smoking, whereas postnatal maternal smoking was positively associated with asthma (odds ratio [OR] = 2.8; 95% confidence interval [CI], 1.3 to 6.1). A negative association between prenatal maternal smoking and atopy was found (OR = 0.6; 95% CI, 0.3 to 0.9). We found no significant association between BHR and parental smoking. Our results indicate that postnatal maternal smoking increases the prevalence of asthma in the offspring without inducing BHR.
Article
Full-text available
A survey was carried out on respiratory symptoms and skin prick test response to common allergens (atopy), storage mites, and occupational allergens among 226 bakers and pastry makers from 105 small businesses in northern Italy. Atopy was present in 54 workers (23.4%); 40 workers (17.7%) were skin positive to at least one storage mite, 27 (11.9%) to wheat flour and 17 (7.5%) to alpha-amylase. Work related asthma was reported by 11 (4.9%) workers and rhinoconjunctivitis by 31 (17.7%); 22 workers (10.2%) complained of chronic bronchitis. The distribution of skin prick test results among bakers and among 119 white collar workers did not indicate (by logistic analysis) an increased risk for bakers to skin sensitisation to common allergens, storage mite, or to a group of five flours. Sensitisation to wheat flour, on the other hand, was present only among exposed workers. Skin sensitisation to occupational allergens was significantly associated with atopy (p < 0.001), smoking habit (p = 0.015), and work seniority (p = 0.027). The risk of work related symptoms was associated with sensitisation to wheat or alpha-amylase, and with atopy, but not with sensitisation to storage mites, work seniority, or smoking habit. The results of the study indicate that there is still a significant risk of allergic respiratory disease among Italian bakers. Not only wheat allergens, but also alpha-amylase must be considered as causative agents, although sensitisation to storage mites is not important in the occupational allergic response. Atopy must be regarded as an important predisposing factor for skin sensitisation to occupational allergens and for the onset of symptoms at work. The data confirm that for effective prevention, greater care should be taken not only in limiting environmental exposure, but also in identifying susceptible people.
Article
Full-text available
To assess the incidence of allergy to complex platinum salts in a platinum refinery. A historical prospective cohort study was carried out on 77 workers (67 men) who started work between 1 January 1979 and 31 December 1991 and who were not atopic on skin prick tests to three common allergens at the time of recruitment. Skin prick tests with complex platinum salts were carried out and diagnosis of allergy to complex platinum salts made by the company's doctor. Skin tests and medical examinations were carried out routinely every six months. Follow up was until 30 September 1992 or until leaving refinery work. 18 workers developed a positive result on skin tests and 23 developed symptoms, including all 18 subjects with positive skin tests; the probability of surviving (95% confidence interval (95% CI)) for 72 months after joining the company, with negative skin test results was 0.67 (0.51-0.79) or with no symptoms was 0.63 (0.49-0.75). The incidence of positive skin tests and symptoms was highest during the first two years of work. Symptoms occurred more frequently in September and October than during the other months of the year. The exclusion of atopic subjects did not seem to have resulted in a lower incidence of sensitisation. Smoking was a significant predictive factor for both positive skin tests (estimated relative risk 5.53) and symptoms (4.70). The findings confirm that smoking is and that atopy may not be a high risk factor for the development of allergy to complex platinum salts. The high incidence of sensitisation and the available data on the clinical course of sensitised workers show that sensitised workers must be promptly and completely removed from exposure.
Article
Full-text available
Within the framework of the SAPALDIA survey (Swiss study on Air Pollution and Lung Diseases in Adults), we studied the influence of sex, age and smoking habits on total serum IgE and allergen-specific IgE antibody concentrations (assessed by means of the Phadiatop® test) and on the prevalence of hay fever. A total of 8,344 subjects aged 18–60 years, comprising 2,776 current smokers, 1,888 former smokers and 3,680 nonsmokers, were included in the study. Smokers had both a statistically significant (p 100 kU/l) than nonsmokers (27.2 kU/l; respectively 20.5%). The IgE level was significantly lower in women than men (p 100 kU/l: atopy probable). In multivariate logistic regression models, the prevalence of positive Phadiatop tests, positive skin tests, and atopy decreased significantly with age. The odds of having a positive Phadiatop and skin test, or being atopic were found to decrease on average by 23.0, 21.1 and 21.0%, respectively, with every 10-year increase in age. With respect to smoking status, the odds ratios for the three atopic markers were significantly lower in current and former smokers than in non-smokers. The prevalence of (self-reported) hay fever was highest in nonsmokers, intermediate in former smokers (odds ratio = 0.81, p
Article
Full-text available
A systematic review was conducted of the effects of parental smoking on immunoglobulin (IgE) levels, skin prick positivity, and allergic rhinitis or eczema in children. Asthma was excluded in order to distinguish more clearly the effect of passive smoke exposure on allergic sensitisation. Thirty six relevant publications were identified after consideration of 692 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 nine studies of IgE in neonates, eight of IgE in older children, 12 which included skin prick tests, and 10 describing symptoms of allergic disease other than asthma or wheezing. A quantitative meta-analysis was possible only for the studies reporting skin prick tests. Several large studies failed to confirm early reports of a substantial or statistically significant association of maternal smoking with concentrations of total serum IgE in neonates or in older children. No consistent association emerged between parental smoking and allergic rhinitis or eczema. Few of these studies adjusted for potential confounding variables. The quantity and quality of evidence was greatest for skin prick tests, and studies of parental smoking during pregnancy or infancy were broadly consistent in showing no adverse effect on prick positivity (pooled odds ratio 0.87, 95% confidence interval 0.62 to 1.24). There was much greater and statistically significant (p = 0.002) heterogeneity of odds ratios relating current parental smoking to skin prick positivity. Parental smoking, either before or immediately after birth, is unlikely to increase the risk of allergic sensitisation in children.
Article
Full-text available
There is evidence that the prevalence of allergies and asthma differs between populations in western and eastern Europe. This study investigated the prevalence of wheezing, rhinitis and eczema among schoolchildren in urban and rural areas of Scandinavia and the formerly socialist countries of Eastern Europe. A total of 79,000 children from two age groups (13-14 yrs and 6-7 yrs) in 18 study centres responded to a questionnaire within the International Study of Asthma and Allergy in Children (ISAAC). The 12 month period prevalence of symptoms of asthma, allergic rhinoconjunctivitis and atopic eczema was calculated. The prevalence of wheezing among the 13-14 yr old children was 11.2-19.7% in Finland and Sweden, 7.6-8.5% in Estonia, Latvia and Poland and 2.6-5.9% in Albania, Romania, Russia, Georgia and Uzbekistan (except Samarkand). The prevalence of itching eyes and flexural dermatitis varied in a similar manner between the three regions. The regional differences were less pronounced among the 6-7 yr old children in the seven participating centres. The highest prevalence of rhinitis was recorded in April-July in Scandinavia and during the winter months in the other countries. The prevalence of atopy-related disorders was higher in Scandinavia than in Estonia, Latvia and Poland, which in turn had a higher prevalence than five other countries of eastern Europe with a culture less similar to western Europe. This supports the hypothesis that "Western life style" is associated with a high prevalence of childhood allergy.
Article
Full-text available
Two recent reviews have assessed the effect of parental smoking on respiratory disease in children. The results of the systematic quantitative review published as a series in Thorax are summarised and brought up to date by considering papers appearing on Embase or Medline up to June 1998. The findings are compared with those of the review published recently by the Californian Environmental Protection Agency (EPA). Areas requiring further research are identified. Overall there is a very consistent picture with odds ratios for respiratory illnesses and symptoms and middle ear disease of between 1.2 and 1.6 for either parent smoking, the odds usually being higher in pre-school than in school aged children. For sudden infant death syndrome the odds ratio for maternal smoking is about 2. Significant effects from paternal smoking suggest a role for postnatal exposure to environmental tobacco smoke. Recent publications do not lead us to alter the conclusions of our earlier reviews. While essentially narrative rather than systematic and quantitative, the findings of the Californian EPA review are broadly similar. In addition they have reviewed studies of the effects of environmental tobacco smoke on children with cystic fibrosis and conclude from the limited evidence that there is a strong case for a relationship between parental smoking and admissions to hospital. They also review data from adults of the effects of acute exposure to environmental tobacco smoke under laboratory conditions which suggest acute effects on spirometric parameters rather than on bronchial hyperresponsiveness. It seems likely that such effects are also present in children. Substantial benefits to children would arise if parents stopped smoking after birth, even if the mother smoked during pregnancy. Policies need to be developed which reduce smoking amongst parents and protect infants and young children from exposure to environmental tobacco smoke. The weight of evidence is such that new prevalence studies are no longer justified. What are needed are studies which allow comparison of the effects of critical periods of exposure to cigarette smoke, particularly in utero, early infancy, and later childhood. Where longitudinal studies are carried out they should be analysed to look at the way in which changes in exposure are related to changes in outcome. Better still would be studies demonstrating reversibility of adverse effects, especially in asthmatic subjects or children with cystic fibrosis.
Article
Objective. To evaluate the impact of adult tobacco use on the health of children. Design. A literature review identified relevant research reports. Meta-analysis was used to compute a pooled risk ratio for each condition studied. The risk ratios were combined with data on exposure rates to produce estimates of the population-attributable risk. Results. Each year, among American children, tobacco is associated with an estimated 284 to 360 deaths from lower respiratory tract illnesses and fires initiated by smoking materials, more than 300 fire-related injuries, 354 000 to 2.2 million episodes of otitis media, 5200 to 165 000 tympanostomies, 14 000 to 21 000 tonsillectomies and/or adenoidectomies, 529 000 physician visits for asthma, 1.3 to 2 million visits for coughs, and in children younger than 5 years of age, 260 000 to 436 000 episodes of bronchitis and 115 000 to 190 000 episodes of pneumonia. Conclusions. The use of tobacco products by adults has an enormous adverse impact on the health of children. Although more research is needed in several areas, action to reduce the morbidity and mortality among childdren should not be delayed. New laws and policies are needed to grant children protection from bodily injury and death attributable to the use of tobacco products by others.
Article
Background-Two recent reviews have assessed the effect of parental smoking on respiratory disease in children. Methods-The results of the systematic quantitative review published as a series in Thorax are summarised and brought up to date by considering papers appearing on Embase or Medline up to June 1998. The findings are compared with those of the review published recently by the Californian Environmental Protection Agency (EPA). Areas requiring further research are identified. Results-Overall there is a very consistent picture with odds ratios for respiratory illnesses and symptoms and middle ear disease of between 1.2 and 1.6 for either parent smoking, the odds usually being higher in pre-school than in school aged children. For sudden infant death syndrome the odds ratio for maternal smoking is about 2. Significant effects from paternal smoking suggest a role for postnatal exposure to environmental tobacco smoke. Recent publications do not lead us to alter the conclusions of our earlier reviews. While essentially narrative rather than systematic and quantitative, the findings of the Californian EPA review are broadly similar. In addition they have reviewed studies of the effects of environmental tobacco smoke on children with cystic fibrosis and conclude from the Limited evidence that there is a strong case for a relationship between parental smoking and admissions to hospital. They also review data from adults of the effects of acute exposure to environmental tobacco smoke under laboratory conditions which suggest acute effects on spirometric parameters rather than on bronchial hyperresponsiveness. It seems likely that such effects are also present in children. Conclusions-Substantial benefits to children would arise if parents stopped smoking after birth, even if the mother smoked during pregnancy. Policies need to be developed which reduce smoking amongst parents and protect infants and young children from exposure to environmental tobacco smoke. The weight of evidence is such that new prevalence studies are no longer justified. What are needed are studies which allow comparison of the effects of critical periods of exposure to cigarette smoke, particularly in utero, early infancy, and later childhood. Where longitudinal studies are carried out they should be analysed to look at the way in which changes in exposure are related to changes in outcome. Better still would be studies demonstrating reversibility of adverse effects, especially in asthmatic subjects or children with cystic fibrosis.
Article
Information on hay fever, eczema, urticaria, respiratory symptoms, smoking habits and occupational dust or gas exposure was obtained by a self-administered questionnaire from a random sample of 4992 subjects of the general population aged 15–70 years of the Hordaland county, Norway. The response rate was 90% of the sample. The lifetime prevalences of hay fever, eczema and urticaria were 10%, 25% and 9% of the respondents, respectively. Eczema and urticaria were more often reported by women than by men. The lifetime prevalence of hay fever decreased substantially by age in both sexes. A history of hay fever was inversely related to cigarette smoking. The lifetime prevalences of eczema and urticaria were associated with occupational dust or gas exposure after adjusting for sex, age, smoking habits and area of residence. Adjusted odds ratios of respiratory symptoms in subjects with hay fever were almost 2.0 compared with those without.
Article
An abstract is unavailable. This article is available as HTML full text and PDF.
Article
Trends in age-standardized death certification rates from all causes, coronary heart disease (CHD), cerebrovascular diseases, all neoplasms and lung cancer were analysed over the period 1980-1993 in 20 major European countries. There were steady and substantial declines of overall mortality in all western European countries for both sexes, although appreciable geographic differences persisted. These favourable trends reflect a decline in CHD mortality in most western countries, besides a persisting fall in cerebrovascular disease, and a substantial stability (with some decline in a few northern and central European countries) in cancer mortality. In contrast, in eastern European countries appreciable rises were registered in mortality from major causes of death considered for males. For females, only moderate declines were observed in Eastern Europe. In the early 1990s, overall mortality was 30 to 100% higher for males and 20 to 100% higher for females as compared to Western Europe. As indicated by the trends in lung cancer death rates, this reflects a major impact of the tobacco-related disease epidemic in subsequent cohorts, as well as more unfavourable lifestyle factors (i.e. aspects of diet, other environmental factors), and a delayed control of hypertension in Eastern Europe, together with a substantial excess of suicides, (road) accidents, homicides and alcohol-related diseases, and the delayed introduction of rational treatment for some conditions. An indication of reversal of mortality trends was evident in the early 1990s only in Poland. In conclusion, there is ample scope for intervention on avoidable mortality in eastern European countries.
Article
Information on hay fever, eczema, urticaria, respiratory symptoms, smoking habits and occupational dust or gas exposure was obtained by a self-administered questionnaire from a random sample of 4992 subjects of the general population aged 15-70 years of the Hordaland county, Norway. The response rate was 90% of the sample. The lifetime prevalences of hay fever, eczema and urticaria were 10%, 25% and 9% of the respondents, respectively. Eczema and urticaria were more often reported by women than by men. The lifetime prevalence of hay fever decreased substantially by age in both sexes. A history of hay fever was inversely related to cigarette smoking. The lifetime prevalences of eczema and urticaria were associated with occupational dust or gas exposure after adjusting for sex, age, smoking habits and area of residence. Adjusted odds ratios of respiratory symptoms in subjects with hay fever were almost 2.0 compared with those without.
Article
This study examined data from three cross sectional surveys of 296 laboratory workers exposed to small mammals. Four indices of laboratory animal allergy were studied: symptoms suggestive of occupational asthma, symptoms suggestive of any occupational allergy, skin weals to animal urine extracts, and serum binding in radioallergosorbent tests with urine extracts. Pooled data from the three surveys showed an association between smoking and all indices except radioallergosorbent tests; the association was significant for symptoms of occupational asthma. One of the three surveys consistently showed a stronger association of allergy indices with smoking than with atopy (defined on skin tests with non-animal aeroallergens). Associations with smoking persisted after stratifying by atopic status, suggesting that smoking may be a risk factor for laboratory animal allergy.
Article
The prevalence of positive skin prick tests (SPT) for common allergens and symptoms of allergic rhinoconjunctivitis or asthma was investigated in Umeå in northern Sweden in 1987. Skin prick tests with 10 allergens common in Sweden and a questionnaire were used to examine 1112 teenagers. All subjects with a positive skin prick test or symptoms were interviewed, and they were further investigated by a serum specific IgE test, a ventilatory lung function test, and a physical examination. At least one skin prick test was positive in 43% of the subjects. Ninety-three percent had at least one positive skin prick test to one of the three most common allergens: cat, timothy grass, and birch. The prevalence of current allergic rhinoconjunctivitis was 17%, current allergic asthma 2.8%, and current asthma (both allergic and nonallergic) 6.8%. Multiple logistic regression analysis showed that the most important risk factors for current asthma were sex (being a girl) and atopy. Heredity of asthma or rhinoconjunctivitis and being born in the winter (October-March) also increased the risk. In atopic subjects, having a mother who smoked and heredity of asthma increased the risk. For allergic rhinoconjunctivitis, heredity increased the risk of getting rhinoconjunctivitis.
Article
The aim of the study was to describe four health related lifestyle characteristics--smoking, exercise, alcohol and food consumption--among Finnish men in 1982-1990. How do unhealthy patterns of behaviour vary according to socio-demographic factors, and do they aggregate or accumulate? The data was compiled in connection with a larger programme entitled 'Monitoring Health Behaviour among the Finnish Adult Population' and conducted by the National Public Health Institute. In the programme a postal questionnaire has been sent annually to a random sample of Finns (N = 5000, resp. rate 70-85%). In this paper, food consumption patterns are described by the use of butter, high-fat milk, coffee sugar and vegetables. The other patterns of behaviour are each measured by one variable. The degree of accumulation is analyzed by comparing the observed and expected (assuming independent occurrence) proportions for simultaneous occurrence of 3-4 unhealthy behaviour patterns. The proportion of men displaying 3-4 unhealthy behaviour patterns has decreased, mostly because of dietary changes. The majority of the men belonged to the intermediate group of 1-2 unhealthy behaviour patterns, and their proportion remained practically unchanged throughout the study period. Unhealthy behaviour was more common in lower educational groups, especially among middle-aged (30-49) and divorced men with a low educational level. Despite the decreasing prevalence of unhealthy behaviour, the degree of accumulation did not change. Accumulation of unhealthy behaviour was much less pronounced among non-smokers than among smokers. This implies that smokers are consistent in their unhealthy behaviour. Smoking might be the gateway to an unhealthy lifestyle in general.
Article
To investigate the relation between skin test reactivity in children and number of siblings. Cross sectional survey among schoolchildren aged 9-11 years. Skin prick tests in the children and self completion of written questionnaire by their parents. 5030 children in Munich and 2623 children in Leipzig and Halle, Germany. Atopic status assessed by skin prick tests. After possible confounders were controlled for, the prevalence of atopic sensitisation decreased linearly with increasing number of siblings (odds ratio = 0.96 for one sibling, 0.67 for five or more siblings; P = 0.005). In atopic children the severity of the skin test reaction as assessed by the weal size was not associated with the number of siblings. Factors directly or indirectly related to the number of siblings may decrease the susceptibility of children to become atopic. Thus, declining family size may in part contribute to the increased prevalence of atopic diseases reported in Western countries over the past few decades.
Article
Smoking, overweight and physical inactivity are three lifestyle risk factors associated with increased risks of cancer, heart disease and other chronic diseases. Using data from the 1985 and 1991 General Social Surveys, this study examines the prevalence of these risk factors by respondents' education levels, and how the prevalence of these risk factors changed from 1985 to 1991. The prevalence of smoking, overweight and physical inactivity varied widely by respondent's education levels. In 1991, persons with more education had consistently lower rates for all three risk factors than those with lower educational levels. Smoking and sedentary living declined between 1985 and 1991, but the prevalence of overweight increased. However, except for physical activity, little progress was made in narrowing the socio-economic differences for these risks. Declines in the prevalence of health risks varied by educational level and by sex within educational level. This has implications for future patterns of chronic disease morbidity and mortality. Differences in risk factor prevalence between socioeconomic groups may be partly due to differences in how each group acquires and interprets health information, and to differences between groups' exposure to environments that support healthy lifestyles.
Article
To evaluate the impact of adult tobacco use on the health of children. A literature review identified relevant research reports. Meta-analysis was used to compute a pooled risk ratio for each condition studied. The risk ratios were combined with data on exposure rates to produce estimates of the population-attributable risk. Each year, among American children, tobacco is associated with an estimated 284 to 360 deaths from lower respiratory tract illnesses and fires initiated by smoking materials, more than 300 fire-related injuries, 354,000 to 2.2 million episodes of otitis media, 5200 to 165,000 tympanostomies, 14,000 to 21,000 tonsillectomies and/or adenoidectomies, 529,000 physician visits for asthma, 1.3 to 2 million visits for coughs, and in children younger than 5 years of age, 260,000 to 436,000 episodes of bronchitis and 115,000 to 190,000 episodes of pneumonia. The use of tobacco products by adults has an enormous adverse impact on the health of children. Although more research is needed in several areas, action to reduce the morbidity and mortality among children should not be delayed. New laws and policies are needed to grant children protection from bodily injury and death attributable to use of tobacco products by others.
Article
Most discussions of statistical methods focus on accounting for measured confounders and random errors in the data-generating process. In observational epidemiology, however, controllable confounding and random error are sometimes only a fraction of the total error, and are rarely if ever the only important source of uncertainty. Potential biases due to unmeasured confounders, classification errors, and selection bias need to be addressed in any thorough discussion of study results. This paper reviews basic methods for examining the sensitivity of study results to biases, with a focus on methods that can be implemented without computer programming. Sensitivity analysis is helpful in obtaining a realistic picture of the potential impact of biases.
Article
Several surveys in children and adults have shown significantly lower prevalences of asthma and allergic diseases in eastern Europe than in western countries. In the former East Germany tremendous changes towards western lifestyle have occurred since unification. The aim of this survey was to investigate time trends in the prevalence of asthma and allergic diseases among children living in the eastern part of Germany. In 1995-96, 2334 (87.5%) schoolchildren in Leipzig participated in a cross-sectional study that used the same methods as a previous survey done shortly after the fall of communism in 1991-92. A self-administered questionnaire was distributed to the parents. Children underwent cold-air challenge and allergy skinprick tests to six common aeroallergens. The prevalence of hay fever (2.3% [34/1454] vs 5.1% [115/2252], p<0.0001) and atopic sensitisation (19.3% [252/1303] vs 26.7% [434/1624], p<0.0001) increased significantly between 1991-92 and 1995-96. However, there was no significant change in the prevalence of asthma, asthma-related symptoms, or bronchial hyper-responsiveness. These findings suggest important differences in the development of atopic disorders. The children were born about 3 years before unification and were therefore exposed to western living conditions only after the third birthday. Thus, factors operating very early in life may be particularly important for the acquisition of childhood asthma, whereas the development of atopic sensitisation and hay fever may also be affected by environmental factors occurring beyond infancy.
Article
Hierarchical models can provide more reasonable and stable parameter estimates than conventional analytical approaches. This technique also deals with problems of multiple comparisons and allows one to model multilevel data within a hierarchical framework. Hence, one would anticipate a surge in applying hierarchical models to epidemiologic data. Difficulties in fitting hierarchical models, however, seem to have limited their use. To help address this problem, we describe the existing software packages that one can use to fit hierarchical models. Since these packages have limited familiarity and applicability in epidemiology, we also present SAS code for analyzing epidemiologic data with hierarchical models. These results allow epidemiologists to fit hierarchical models with readily available software.
Skin test reactivity and number of siblings
  • E Von Mutius
  • F Martinez
  • C Fritzsch
  • T Nicolai
  • P Reitmar
  • H Thiemann
von Mutius E, Martinez F, Fritzsch C, Nicolai T, Reitmar P, Thiemann H. Skin test reactivity and number of siblings. Lancet 1994; 308:692±5.
  • Hurt RD
Respiratory symptoms and atopic sensitization among school children around different settings around the Baltic sea
  • Bråbäckl