Results from the European Union MAPEC_LIFE cohort study on air pollution and chromosomal damage in children: are public health policies sufficiently protective?

Background: Children are at high risk of suffering health consequences of air pollution and childhood exposure can increase the risk of developing chronic diseases in adulthood. This study, part of the MAPEC_LIFE project (LIFE12 ENV/IT/000614), aimed to investigate the associations between exposure to urban air pollutants and micronucleus (MN) frequency, as a biomarker of chromosomal damage, in buccal cells of children for supporting implementation and updating of environmental policy and legislation. Methods: This prospective epidemiological cohort study was carried out on 6- to 8-year-old children living in five Italian towns with different levels and features of air pollution. Exfoliated buccal cells of the children were sampled twice, in winter and spring, obtaining 2139 biological samples for genotoxicological investigation. Micronucleus (MN) frequency was investigated in buccal cells of children and its association with air pollution exposure was assessed applying multiple Poisson regression mixed models, including socio-demographic and lifestyle factors as confounders. We also dichotomize air pollutants\u2019 concentration according to the EU Ambient Air Quality Directives and WHO Air Quality Guidelines in all Poisson regression models to assess their risk predictive capacity. Results: Positive and statistically significant associations were found between MN frequency and PM10, PM2.5, benzene, SO2 and ozone. The increment of the risk of having MN in buccal cells for each \u3bcg/m3 increase of pollutant concentration was maximum for benzene (18.9%, 95% CIs 2.2\u201338.4%) and modest for the other pollutants (between 0.2 and 1.4%). An increased risk (between 17.9% and 59.8%) was found also for exposure to PM10, benzene and benzo(a)pyrene levels higher than the threshold limits. Conclusions: Some air pollutants are able to induce chromosomal damage in buccal cells of children even at concentrations below present EU/WHO limits. This type of biological effects may be indicative of the environmental pressure which populations are exposed to in urban areas

Adrenergic receptor gene polymorphism and left ventricular reverse remodelling after cardiac resynchronization therapy: preliminary results

AIMS: Several factors can influence the extent of left ventricular (LV) reverse remodelling after cardiac resynchronization therapy (CRT) in patients with heart failure (HF). Polymorphism in genes involved in cardiac remodelling, namely beta-adrenergic receptors (ARs), may have a role. We studied the influence of beta-1 Arg389Gly, beta-2 Arg16Gly, and beta-2 Gln27Glu ARs gene polymorphisms on the magnitude of reverse remodelling response to CRT and its possible correlations with the incidence of appropriate implantable cardioverter-defibrillator (ICD) shocks. METHODS AND RESULTS: Beta-ARs were assessed in 101 patients with HF due to idiopathic (50.5%) or ischaemic (49.5%) dilated cardiomyopathy, undergoing CRT for standard indications [left ventricular ejection fraction (LVEF) 23.5 ± 7.5%, QRS ≥ 120 ms]. Left ventricular ejection fraction was measured by echocardiography at baseline, 6 months after CRT, and periodically afterwards. The LVEF change from baseline was of 3.1 ± 11 units among Gln27Gln, 8.3 ± 10.4 units among Gln27Glu, 11 ± 6.4 units among Glu27Glu carriers (P = 0.018 for Gln27Gln vs. Glu27Glu carriers), and 8.8 ± 9.8 units among Gln27Glu + Glu27Glu carriers (P = 0.006 vs. Gln27Gln). Gln27 homozygotes had a higher incidence of appropriate ICD shocks for fast ventricular tachycardia/ventricular fibrillation. CONCLUSION: Beta-2 Gln27Glu ARs gene polymorphism may influence LV reverse remodelling after CRT with Glu27Glu carriers showing the greatest improvement. It may also influence the incidence of malignant ventricular tachyarrhythmias