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Ambient air pollution (AAP) is recognized a cardiovascular risk factor and lipid profile dysregulation seems to be one of the potential mediators involved. However, results from epidemiologic research on the association between exposure to AAP and altered lipid profile have been inconsistent. This study aims to systematically review and meta-analyse epidemiologic evidence on the association between exposure to ambient air pollutants (particulate matter, nitrogen oxides, sulphur dioxide, ozone, carbon monoxide, back carbon) and lipid profile parameters (Total cholesterol; High-Density Lipoprotein Cholesterol; Low-Density Lipoprotein Cholesterol; TG-Triglycerides) or dyslipidaemia.Systematic electronic literature search was performed in PubMed, Web of Science and Scopus databases (last search on 24th May 2019) using keywords related to the exposure (ambient air pollutants) and to the outcomes (lipid profile parameters/dyslipidaemia). Qualitative and quantitative information of the studies were extracted and fixed or random-effects models were used to obtain a pooled effect estimate per each pollutant/outcome combination.22 studies were qualitatively analysed and, from those, 3 studies were quantitatively analysed. Particulate matters were the most studied pollutants and a considerable heterogeneity in air pollution assessment methods and outcomes definitions was detected. Age, obesity related measures, tobacco consumption, sex and socioeconomic factors were the most frequent considered variables for confounding adjustment in the models. In a long-term exposure scenario, we found a 3.14% (1.36%e4.95%) increase in TG levels per 10 mg/m 3 PM 10 increment and a 4.24% (1.37%e7.19%) increase in TG levels per 10 mg/m 3 NO 2 increment. No significant associations were detected for the remaining pollutant/outcome combinations.Despite the few studies included in the meta-analysis, our study suggests some epidemiologic evidence supporting the association between PM 10 and NO 2 exposures and increased TG levels. Due to the very low level of evidence, more studies are needed to clarify the role of lipid profile dysregulation as a mediator on the AAP adverse cardiovascular effects.

INSEF has set up an experienced national and regional structure for HES implementation. Nationally representative quality epidemiological data is now available for public health monitoring, planning and research.

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BackgroundMetabolic syndrome (MetS) is a cluster of conditions that occur together, increasing the risk of heart disease, stroke and diabetes. Since pathways implicated in different diseases reveal surprising insights into shared genetic bases underlying apparently unrelated traits, we hypothesize that there are common genetic components involved in the clustering of MetS traits. With the aim of identifying these common genetic components, we have performed a genetic association study by integrating MetS traits in a continuous MetS score.MethodsA cross-sectional study developed in the context of the Portuguese Component of the European Health Examination Survey (EHES) was used. Data was collected through a detailed questionnaire and physical examination. Blood samples were collected and biochemical analyses were performed. Waist circumference, blood pressure, glucose, triglycerides and high density lipoprotein cholesterol (HDL) levels were used to compute a continuous MetS score, obtained by Principal Component Analysis. A total of 37 single nucleotide polymorphisms (SNPs) were genotyped and individually tested for association with the score, adjusting for confounding variables.ResultsA total of 206 individuals were studied. Calculated MetS score increased progressively with increasing number of risk factors (P < 0.001). We found a significant association between CYP2C19 rs4244285 and the MetS score not detected using the MetS dichotomic approach. Individuals with the A allelic variant seem to be protected against MetS, displaying a lower MetS score (Mean difference: 0.847; 95%CI: 0.163-1.531; P = 0.015), after adjustment for age, gender, smoking status, excessive alcohol consumption and physical inactivity. An additive genetic effect of GABRA2 rs279871, NPY rs16147 and TPMT rs1142345 in the MetS score variation was also found.ConclusionsThis is the first report of a genetic association study using a continuous MetS score. The significant association found between the CYP2C19 polymorphism and the MetS score but not with the individual associated traits, emphasizes the importance of lipid metabolism in a MetS common etiological pathway and consequently on the clustering of different cardiovascular risk factors. Despite the sample size limitation of our study, this strategy can be useful to find genetic factors involved in the etiology of other disorders that are defined in a dichotomized way.