25 research outputs found
Maternal smoking during pregnancy increases the risk of recurrent wheezing during the first years of life (BAMSE)
BACKGROUND: Exposure to cigarette smoking during foetal and early postnatal life may have implications for lung health. The aim of this study was to assess the possible effects of such exposure in utero on lower respiratory disease in children up to two years of age. METHODS: A birth cohort of 4089 newborn infants was followed for two years using parental questionnaires. When the infant was two months old the parents completed a questionnaire on various lifestyle factors, including maternal smoking during pregnancy and after birth. At one and two years of age information was obtained by questionnaire on symptoms of allergic and respiratory diseases as well as on environmental exposures, particularly exposure to environmental tobacco smoke (ETS). Adjustments were made for potential confounders. RESULTS: When the mother had smoked during pregnancy but not after that, there was an increased risk of recurrent wheezing up to two years' age, OR(adj )= 2.2, (95% CI 1.3 – 3.6). The corresponding OR was 1.6, (95% CI 1.2 – 2.3) for reported exposure to ETS with or without maternal smoking in utero. Maternal smoking during pregnancy but no exposure to ETS also increased the risk of doctor's diagnosed asthma up to two years of age, OR(adj )= 2.1, (95% CI 1.2 – 3.7). CONCLUSION: Exposure to maternal cigarette smoking in utero is a risk factor for recurrent wheezing, as well as doctor's diagnosed asthma in children up to two yearsof age
Izloženost ambijentalnomu duhanskomu dimu na radnome mjestu u Makedoniji: kako sada stojimo?
To assess the prevalence and the level of exposure to environmental tobacco smoke (ETS) in the workplace after the enactment of the law restricting indoor smoking in Macedonia, we performed a cross-sectional, self-administered questionnaire study including 372 never-smoking workers recruited from six workplaces. We found a high prevalence of workers exposed to ETS in the workplace (27.4 %) with no significant difference between particular occupation groups. We found no significant difference in the prevalence of passive smokers in the workplace between this study and our study conducted before the law was enacted (31.5 % vs. 27.4 %, P=0.324). The prevalence of workers exposed to ETS for less than three hours a day was significantly lower than of passive smokers with longer exposure (28.4 % vs. 71.6 %, P=0.038). The prevalence of workers exposed to ETS from less than 10 cigarettes smoked by coworkers per day was lower than the prevalence of workers with higher exposure, but statistical significance was not reached (37.9 % vs. 62.1 %, P=0.087). Our findings indicate a high prevalence and a high level of exposure to ETS in the workplace, which calls for stricter adherence to smoking-free legislation or even the total ban of smoking in the workplace.Ovo je ispitivanje obuhvatilo 372 radnika na šest različitih radnih mjesta koji nikad nisu pušili kako bi se procijenila zastupljenost osoba izloženih duhanskomu dimu na radnome mjestu i razina njihove izloženosti nakon zakonskih ograničenja pušenja u zatvorenim prostorijama u Makedoniji. Ispitivanje je provedeno s pomoću upitnika koji su radnici ispunjavali sami. Utvrdili smo visoku zastupljenost radnika izloženih ambijentalnomu duhanskomu dimu na radnome mjestu (27,4 %) te nisu zamijećene statistički značajne razlike među zanimanjima. Nisu uočene značajne razlike između zastupljenosti pasivnih pušača na radnome mjestu u ovome ispitivanju i u našem ranijem ispitivanju, kada još nije na snagu stupio zakon o ograničenju pušenja (31,5 % naprema 27,4 %, P=0,324). Zastupljenost radnika izloženih ambijentalnomu duhanskomu dimu ne dulje od tri sata na dan bila je statistički značajno niža negoli onih čija je izloženost trajala duže (28,4 % naprema 71,6 %, P=0,038). Zastupljenost radnika koji su bili izloženi dimu kolega koji su pušili manje od 10 cigareta na dan bila je niža negoli onih s većom izloženosti, ali razlika nije bila statistički značajna (37,9 % naprema 62,1 %, P=0,087). Naši rezultati potvrđuju da i dalje postoje visoka zastupljenost izloženih radnika i visoke razine izloženosti ambijentalnomu duhanskomu dimu na radnome mjestu, što upućuje na potrebu uvođenja strožih zakona o zabrani pušenja
The impact of a minimal smoking cessation intervention for pregnant women and their partners on perinatal smoking behaviour in primary health care: A real-life controlled study
<p>Abstract</p> <p>Background</p> <p>There is a demand for strategies to promote smoking cessation in high-risk populations like smoking pregnant women and their partners. The objectives of this study were to investigate parental smoking behaviour during pregnancy after introduction of a prenatal, structured, multi-disciplinary smoking cessation programme in primary care, and to compare smoking behaviour among pregnant women in the city of Trondheim with Bergen and Norway.</p> <p>Methods</p> <p>Sequential birth cohorts were established to evaluate the intervention programme from September 2000 to December 2004 in primary care as a part of the Prevention of Allergy among Children in Trondheim study (PACT). The primary outcome variables were self reported smoking behaviour at inclusion and six weeks postnatal. Data from the Medical Birth Registry of Norway (MBR) were used to describe smoking cessation during pregnancy in Trondheim, Bergen and Norway 1999–2004.</p> <p>Results</p> <p>Maternal smoking prevalence at inclusion during pregnancy were 5% (CI 95% 4–6) in the intervention cohort compared to 7% (CI 95% 6–9), p = 0.03, in the control cohort. Of the pre-pregnancy maternal smokers 25% (CI 95% 20–31) and 32% (CI 95% 26–38), p = 0.17, were still smoking at inclusion in the intervention and control cohorts, respectively. Six weeks postnatal 72% (CI 95% 59–83) and 68% (CI 95% 57–77), p = 0.34 of the maternal smokers at inclusion still smoked. No significant difference in paternal smoking between the cohorts was found after the intervention period. Data from the MBR showed a significantly higher proportion of women who stopped smoking during pregnancy in Trondheim than in Bergen in 2003 and 2004, p = 0.03 and < 0.001, respectively.</p> <p>Conclusion</p> <p>No impact on parental smoking behaviour between the cohorts was observed after the smoking intervention programme. Of the women who stopped smoking during pregnancy most of them stopped smoking before the intervention. However, we observed a significantly higher quitting rate in Trondheim than in Bergen in 2003 and 2004 which may have been facilitated by the supplemental attention on smoking behaviour the PACT study initiated.</p
A primary health-care intervention on pre- and postnatal risk factor behavior to prevent childhood allergy. The Prevention of Allergy among Children in Trondheim (PACT) study
Background: This study aimed to evaluate the impact of a primary prevention intervention program on risk
behavior for allergic diseases among children up to 2 years of age. The setting was in ordinary pre- and postnatal
primary health care in Trondheim, Norway.
Methods: The Prevention of Allergy among Children in Trondheim, Norway (PACT) study invited all pregnant
women and parents to children up to 2 years of age in the community to participate in a non-randomized,
controlled, multiple life-style intervention study. Interventional topics was increased dietary intake of cod liver oil
and oily fish for women during pregnancy and for infants during the first 2 years of life, reduced parental smoking
and reduced indoor dampness. A control cohort was established prior to the intervention cohort with “follow up
as usual”. Questionnaires were completed in pregnancy, 6 weeks after birth and at 1 and 2 years of age. Trends in
exposure and behavior are described.
Results: Intake of oily fish and cod liver oil increased statistically significantly among women and infants in the
intervention cohort compared to the control cohort. There was a low postnatal smoking prevalence in both
cohorts, with a trend towards a decreasing smoking prevalence in the control cohort. There was no change in
indoor dampness or in behavior related to non- intervened life-style factors.
Conclusions: The dietary intervention seemed to be successful. The observed reduced smoking behavior could
not be attributed to the intervention program, and the latter had no effect on indoor dampness
Fetal and infant origins of asthma
Previous studies have suggested that asthma, like other common diseases, has at least part of its origin early in life. Low birth weight has been shown to be associated with increased risks of asthma, chronic obstructive airway disease, and impaired lung function in adults, and increased risks of respiratory symptoms in early childhood. The developmental plasticity hypothesis suggests that the associations between low birth weight and diseases in later life are explained by adaptation mechanisms in fetal life and infancy in response to various adverse exposures. Various pathways leading from adverse fetal and infant exposures to growth adaptations and respiratory health outcomes have been studied, including fetal and early infant growth patterns, maternal smoking and diet, children’s diet, respiratory tract infections and acetaminophen use, and genetic susceptibility. Still, the specific adverse exposures in fetal and early postnatal life leading to respiratory disease in adult life are not yet fully understood. Current studies suggest that both environmental and genetic factors in various periods of life, and their epigenetic mechanisms may underlie the complex associations of low birth weight with respiratory disease in later life. New well-designed epidemiological studies are needed to identify the specific underlying mechanisms. This review is focused on specific adverse fetal and infant growth patterns and exposures, genetic susceptibility, possible respiratory adaptations and perspectives for new studies
Mouse models to unravel the role of inhaled pollutants on allergic sensitization and airway inflammation
Air pollutant exposure has been linked to a rise in wheezing illnesses. Clinical data highlight that exposure to mainstream tobacco smoke (MS) and environmental tobacco smoke (ETS) as well as exposure to diesel exhaust particles (DEP) could promote allergic sensitization or aggravate symptoms of asthma, suggesting a role for these inhaled pollutants in the pathogenesis of asthma. Mouse models are a valuable tool to study the potential effects of these pollutants in the pathogenesis of asthma, with the opportunity to investigate their impact during processes leading to sensitization, acute inflammation and chronic disease. Mice allow us to perform mechanistic studies and to evaluate the importance of specific cell types in asthma pathogenesis. In this review, the major clinical effects of tobacco smoke and diesel exhaust exposure regarding to asthma development and progression are described. Clinical data are compared with findings from murine models of asthma and inhalable pollutant exposure. Moreover, the potential mechanisms by which both pollutants could aggravate asthma are discussed
Effect of Perinatal secondhand tobacco smoke exposure on in vivo and intrinsic airway structure/function in non-human primates
An Update on the Prevalence of Allergic Rhinitis in Korea, and Correlation with Hypertension, Obesity and Smoking
Induction of a disintegrin and metalloprotease 33 during embryonic lung development and the influence of IL-13 or maternal allergy
BackgroundAsthma pathogenesis involves gene and environmental interactions. A disintegrin and metalloprotease 33 (ADAM33)/Adam33 is a susceptibility gene for asthma and bronchial hyperresponsiveness in human beings and mice. ADAM33 is almost exclusively expressed in mesenchymal cells, including mesenchymal progenitors in developing lungs.ObjectiveBecause maternal allergy is a risk factor for asthma, we hypothesized that an allergic environment affects ADAM33/Adam33 expression during human and mouse lung development.MethodsHuman embryonic/fetal lung (HEL) tissues were collected from first-trimester terminations of pregnancy. These were processed immediately or used for explant culture ± IL-13. MF1 mice or ovalbumin-sensitized A/J mice (Bronchial hyperresponsivness (Bhr)1/Adam33 locus–positive) were time-mated and challenged with ovalbumin (A/J mice only) during pregnancy. Lungs were harvested at different times during gestation and post partum. ADAM33/Adam33 expression was analyzed by using reverse transcriptase quantitative polymerase chain reaction and Western blotting.ResultsADAM33 mRNA was detectable in HELs in the pseudoglandular stage of development and showed a significant increase from 7 to 9 weeks postconception. IL-13 significantly suppressed ADAM33 mRNA in HEL explants. In developing murine lungs, Adam33 mRNA and protein expression increased significantly in the early pseudoglandular stage and showed another large increase post partum. In A/J mice, maternal allergy significantly suppressed Adam33 mRNA in lungs of newborn pups, whereas processed Adam33 protein increased and several smaller isoforms were detected.ConclusionAdam33/Adam33 shows 2 significant increments in expression during lung morphogenesis, suggesting important developmental regulation. The ability of maternal allergy or exogenous IL-13 to suppress Adam33/ADAM33 mRNA but enhance Adam33 processing suggests a gene-environment interaction that may be relevant for asthma pathogenesis