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%-4.95%) increase in TG levels per 10 μg/m PM increment and a 4.24% (1.37%-7.19%) increase in TG levels per 10 μg/m NO 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 and NO 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.