Inflammation after diesel exhaust and DEP exposure is evident at higher concentrations only; there appears to be a threshold dose for DEPs approximating 300 μg/m. The lack of a biological response to DEPs at lower concentrations may reflect a contribution of gaseous constituents or interactions between DEPs and gaseous air pollutants to the human inflammatory response and function loss.

Many studies have reported associations between air pollution particles with an aerodynamic diameter <2.5 μm (fine particulate matter (PM)) and adverse cardiovascular effects. However, there is an increased concern that so-called ultrafine PM which comprises the smallest fraction of fine PM (aerodynamic diameter <0.1 μm) may be disproportionately toxic relative to the 0.1-2.5 μm fraction. Ultrafine PM is not routinely measured in state monitoring networks and is not homogenously dispersed throughout an airshed but rather located in hot spots such as near combustion sources (e.g., roads), making it difficult for epidemiology studies to associate exposure to ultrafine PM with adverse health effects. Thirty four middle-aged individuals with metabolic syndrome were exposed for 2 h while at rest in a randomized crossover design to clean air and concentrated ambient ultrafine particles (UCAPS) for 2 h. To further define potential risk, study individuals carrying the null allele for GSTM1 (a prominent antioxidant gene) were identified by genotyping. Blood was obtained immediately prior to exposure, and at 1 and 20 h afterward. Continuous Holter monitoring began immediately prior to exposure and continued for 24 h. Based on changes we observed in previous CAPS studies, we hypothesized that ultrafine CAPS would cause changes in markers of blood inflammation and fibrinolysis as well as changes in heart rate variability and cardiac repolarization. GSTM1 null individuals had altered cardiac repolarization as seen by a change in QRS complexity following exposure to UCAPS and both the entire study population as well as GSTM1 null individuals had increased QT duration. Blood plasminogen and thrombomodulin were decreased in the whole population following UCAPS exposure, whereas C-reactive protein (CRP) and SAA were increased. This controlled human exposure study is the first to show that ambient ultrafine particles can cause cardiovascular changes in people with metabolic syndrome, which affects nearly a quarter of the U.S. adult population.

Context: Exposure to air pollution can result in the onset of arrhythmias.Case presentation: We present a case of a 58-year-old woman who volunteered to participate in a controlled exposure to concentrated ambient particles. Twenty minutes into the exposure, telemetry revealed new onset of atrial fibrillation. The exposure was discontinued, and she reverted to normal sinus rhythm approximately 2 hr later. No abnormality was evident on the volunteer’s laboratory examination or echocardiography that could explain an increased risk for supraventricular arrhythmia.Discussion: Epidemiologic evidence strongly supports a relationship between exposure to air pollutants and cardiovascular disease, but population-level data are not directly relevant to the clinical presentation of individual cases. To our knowledge, this is the only case report of an individual suffering an episode of atrial fibrillation after exposure to an air pollutant. The resolution of the arrhythmia with termination of the particle exposure further supports a causal relationship between the two.Relevance to clinical practice: Exposure to air pollution, including particulate matter, may cause supraventricular arrhythmias.

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