Dose-dependent relationship between prenatal exposure to fine particulates and exhaled carbon monoxide in non-asthmatic children : a population-based birth cohort study

Objectives: The main goal of the study was to assess possible association between fetal exposure to fi ne particulate matter (PM2.5) and exhaled carbon monoxide (eCO) measured in non-asthmatic children. Material and Methods: The subjects include 118 children taking part in an ongoing population-based birth cohort study in Kraków. Personal samplers of PM2.5 were used to measure fi ne particle mass in the fetal period and carbon monoxide (CO) in exhaled breath from a single exhalation effort at the age of 7. In the statistical analysis of the effect of prenatal PM2.5 exposure on eCO, a set of potential confounders, such as environmental tobacco smoke (ETS), city residence area, sensitization to house dust allergens and the occurrence of respiratory symptoms monitored over the seven-year follow-up was considered. Results: The level of eCO did not correlate with the self-reported ETS exposure recorded over the follow-up, however, there was a positive signifi cant relationship with the prenatal PM2.5 exposure (non-parametric trend p = 0.042). The eCO mean level was higher in atopic children (geometric mean = 2.06 ppm, 95% CI: 1.58–2.66 ppm) than in non-atopic ones (geometric mean = 1.57 ppm, 95% CI: 1.47–1.73 ppm) and the difference was statistically signifi cant (p = 0.036). As for the respiratory symptoms, eCO values were associated positively only with the cough severity score recorded in the follow-up (nonparametric trend p = 0.057). In the nested multivariable linear regression model, only the effects of prenatal PM2.5 and cough severity recorded in the follow-up were related to eCO level. The prenatal PM2.5 exposure represented 5.1%, while children’s cough represented only 2.6% of the eCO variability. Conclusion: Our study suggests that elevated eCO in non-asthmatic children may result from oxidative stress experienced in the fetal period and that heme oxygenase (HO) activity in body tissues may be programmed in the fetal period by the exposure to fi ne particulate matter

Intrauterine exposure to fine particulate matter as a risk factor for increased susceptibility to acute broncho-pulmonary infections in early childhood

Over the last decades many epidemiologic studies considered the morbidity patterns for respiratory diseases and lung function of children in the context of ambient air pollution usually measured in the postnatal period. The main purpose of this study is to assess the impact of prenatal exposure to fine particulate matter (PM(2.5)) on the recurrent broncho-pulmonary infections in early childhood. The study included 214 children who had measurements of personal prenatal PM(2.5) exposure and regularly collected data on the occurrence of acute bronchitis and pneumonia diagnosed by a physician from birth over the seven-year follow-up. The effect of prenatal exposure to PM(2.5) was adjusted in the multivariable logistic models for potential confounders, such as prenatal and postnatal ETS (environmental tobacco smoke), city residence area as a proxy of postnatal urban exposure, children’s sensitization to domestic aeroallergens, and asthma. In the subgroup of children with available PM(2.5) indoor levels, the effect of prenatal exposure was additionally adjusted for indoor exposure as well. The adjusted odds ratio (OR) for incidence of recurrent broncho-pulmonary infections (five or more spells of bronchitis and/or pneumonia) recorded in the follow-up significantly correlated in a dose-response manner with the prenatal PM(2.5) level (OR = 2.44, 95%CI: 1.12 – 5.36). In conclusion, the study suggests that prenatal exposure to PM(2.5) increases susceptibility to respiratory infections and may program respiratory morbidity in early childhood. The study also provides evidence that the target value of 20 μg/m(3) for the 24-hour mean level of PM(2.5) protects unborn babies better than earlier established EPA guidelines

Antihistamine medication may alleviate negative effects of prenatal exposure to polycyclic aromatic hydrocarbons (PAH) on lung function in children. Birth cohort prospective study

The main purpose of the present study was to test the hypothesis that the depressed lung growth attributable to prenatal exposure to polycyclic aromatic hydrocarbons (PAH) may be modified by the intake of antihistamine medications. Individual prenatal PAH exposure was assessed by personal air monitoring in 176 children who were followed over nine years, in the course of which outdoor residential air monitoring, allergic skin tests for indoor allergens, lung function tests (FVC, FEV(1), FEV(05) and FEF(25-75)) were performed. The analysis with the General Estimated Equation (GEE) showed no association between prenatal PAH exposure and lung function in the group of children who were reported to be antihistamine users. However, in the group of antihistamine non-users all lung function tests except for FEF(25-75) were significantly and inversely associated with prenatal airborne PAH exposure. CONCLUSION: The results of the study suggest that the intake of antihistamine medications in early childhood may inhibit the negative effect of fetal PAH exposure on lung growth and provides additional indirect evidence for the hypothesis that lung alterations in young children resulting from PAH exposure may be caused by the allergic inflammation within lung

Intrauterine exposure to fine particulate matter as a risk factor for increased susceptibility to acute broncho-pulmonary infections in early childhood

Over the last decades many epidemiologic studies considered the morbidity patterns for respiratory diseases and lung function of children in the context of ambient air pollution usually measured in the postnatal period. The main purpose of this study is to assess the impact of prenatal exposure to fine particulate matter (PM(2.5)) on the recurrent broncho-pulmonary infections in early childhood. The study included 214 children who had measurements of personal prenatal PM(2.5) exposure and regularly collected data on the occurrence of acute bronchitis and pneumonia diagnosed by a physician from birth over the seven-year follow-up. The effect of prenatal exposure to PM(2.5) was adjusted in the multivariable logistic models for potential confounders, such as prenatal and postnatal ETS (environmental tobacco smoke), city residence area as a proxy of postnatal urban exposure, children’s sensitization to domestic aeroallergens, and asthma. In the subgroup of children with available PM(2.5) indoor levels, the effect of prenatal exposure was additionally adjusted for indoor exposure as well. The adjusted odds ratio (OR) for incidence of recurrent broncho-pulmonary infections (five or more spells of bronchitis and/or pneumonia) recorded in the follow-up significantly correlated in a dose-response manner with the prenatal PM(2.5) level (OR = 2.44, 95%CI: 1.12 – 5.36). In conclusion, the study suggests that prenatal exposure to PM(2.5) increases susceptibility to respiratory infections and may program respiratory morbidity in early childhood. The study also provides evidence that the target value of 20 μg/m(3) for the 24-hour mean level of PM(2.5) protects unborn babies better than earlier established EPA guidelines