Cardiovascular-related clinical markers were evaluated in this cross-sectional study of United States adults (aged ≥ 20) exposed to lead via the National Health and Nutrition Examination Survey 2007–2008 and the 2009–2010 datasets. In four quartiles of exposure—0–2 μg/dL, 2–5 μg/dL, 5–10 μg/dL, and 10 μg/dL and over, clinical and anthropometric markers were evaluated—to examine how the markers manifested in the quartiles. Associations were determined via linear regression. Finally, clinical makers, and how they manifested between exposed and less-exposed occupations, were explored in addition to how duration of exposure altered these clinical markers. In regression analysis, Diastolic Blood Pressure (DBP) and high-density lipoprotein (HDL) cholesterol, were significantly associated with blood lead level (BLL). In the occupational analysis, Systolic Blood Pressure (SBP), DBP, C-reactive protein (CRP), triglycerides, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, showed differences between populations in the exposed and less-exposed occupations. Regarding Agriculture, Forestry & Fishing, the duration of exposure altered SBP, CRP, and LDL cholesterol. With mining, the duration of exposure altered SBP, DBP, triglycerides, and HDL cholesterol, whereas in construction, the duration in occupation altered SBP, triglycerides, and CRP. In conclusion, lead exposure has a profound effect on the cardiovascular system, with potentially adverse outcomes existing at all exposure levels.

Elemental characterization of fine particulate matter was undertaken at schools and residences in three low income neighborhoods in Quito, Ecuador. The three zones were located in the northern (Cotocollao), south central (El Camal), and south east (Los Chillos) neighborhoods and were classified as zones 1–3, respectively. Forty elements were quantified via ICP-MS analysis. Amongst the geogenic elements, the concentration of Si was the most abundant followed by S, Al, and Ca. Elements with predominantly anthropogenic sources such as Zn, V, and Ni were higher in zone 3 school followed by zone 2 and zone 1 schools. Enrichment factors were calculated to study the role of crustal sources in the elemental concentrations. Geogenic elements, except K, all had values 10. Principal Component Analysis suggested that Ni and V concentrations were strongly attributable to pet coke and heavy oil combustion. Strong associations between As and Pb could be attributed to traffic and other industrial emissions. Resuspended dust, soil erosion, vehicular emissions (tailpipe, brake and tire wear, and engine abrasion), pet coke, heavy oil combustion, and heavy industrial operations were major contributors to air pollution.

Chronic exposure to urban traffic pollution is documented to promote atherosclerosis in adults but little is known about its potential effects in children. Our study examined the association of long-term exposure to traffic with carotid intima-media thickness (cIMT) in 287 healthy children. Residential proximity and distance-weighted traffic density (DWTD) were used as proximity markers for traffic-related air pollution exposure. The multivariable analyses revealed that children residing <100 meters from the nearest heavily trafficked road had cIMT mean and maximum measurements that were increased by 15% and 11% compared to those living ≥ 200 meters away (P=0.0001). Similar increases in cIMT were identified for children in the highest versus lowest DWTD tertile. Children who resided 100–199 meters from traffic or in the middle DWTD tertile also exhibited increased cIMT but these differences were not statistically significant. No statistically significant differences were identified between residential distance to traffic or DWTD and systemic inflammation indicators (CRP, IL-6). The study results suggest that exposure to urban traffic promotes arterial remodeling in children. This finding is important since even small increases in cIMT over time can potentially lead to earlier progression to atherosclerosis. It is also important because traffic-related pollution is potentially modifiable.

Low-grade systemic inflammation is implicated in metabolic syndrome (MetS) and cardiometabolic diseases. Diet is hypothesized to be an important low-grade inflammation modifier. However, few studies have examined the association of dietary inflammation with MetS and cardiometabolic risk in Latin American populations and their findings are inconsistent. Our cross-sectional study examined the association of dietary inflammatory potential with MetS and cardiometabolic risk components in 276 urban Ecuadorian women. Dietary inflammation was evaluated using an energy-adjusted Dietary Inflammatory Index (E-DII), divided into quartiles (Q). E-DII scores ranged from −4.89 (most anti-inflammatory) to 4.45 (most pro-inflammatory). Participants in the most pro-inflammatory (Q4) compared to the least inflammatory E-DII quartile (Q1) had a 4.4 increased adjusted odds for MetS (95% C.I. = 2.0, 9.63; p < 0.001). Every one-unit increase in E-DII was associated with a 1.4 increase in MetS (95% CI = 1.22, 1.52; p < 0.001). In other adjusted models, the most pro-inflammatory E-DII quartile (Q4) was positively associated with total blood cholesterol and triglycerides (p < 0.001), LDL-c (p = 0.007), diastolic blood pressure (p< 0.002), mean arterial pressure (p < 0.006), waist circumference (p < 0.008), and Framingham risk score (p < 0.001). However, the previously identified associations with pulse wave velocity and BMI were no longer evident in the models. These findings suggest that more pro-inflammatory diets may contribute to poorer cardiometabolic health. Promoting healthier diets with a lower inflammatory potential may help to prevent or slow development of cardiometabolic disorders.