Brominated flame retardants (BFRs) are an important group of additives in plastics that increase resistance to ignition and slow down the rate of burning. Because of concerns about their environmental and human health impacts, however, some of the most widely employed BFRs, including hexabromocyclododecane (HBCD) and commercial mixtures of penta-, octa- and deca- (poly)bromodiphenyl ethers (PBDEs), have been restricted or phased out. In this review, the oceanic sources and pathways of PBDEs, the most widely used BFRs, are evaluated and quantified, with particular focus on emissions due to migration from plastics into the atmosphere versus emissions associated with the input of retarded or contaminated plastics themselves. Calculations based on available measurements of PBDEs in the environment suggest that 3.5 and 135 tonnes of PBDEs are annually deposited in the ocean when scavenged by aerosols and through air-water gas exchange, respectively, with rivers contributing a further ∼40 tonnes. Calculations based on PBDE migration from plastic products in use or awaiting or undergoing disposal yield similar net inputs to the ocean but indicate a relatively rapid decline over the next two decades in association with the reduction in the production and recycling of these chemicals. Estimates associated with the input of PBDEs to the ocean when “bound” to marine plastics and microplastics range from about 360 to 950 tonnes per year based on the annual production of plastics and PBDEs over the past decade, and from about 20 to 50 tonnes per annum based on the abundance and distribution of PBDEs in marine plastic litter. Because of the persistence and pervasiveness of plastics in the ocean and diffusion coefficients for PBDEs on the order of 10⁻²⁰ to 10⁻²⁷ m² s⁻¹, microplastics are likely to act as a long-term source of these chemicals though gradual migration. Locally, however, and more important from an ecotoxicological perspective, PBDE migration may be significantly enhanced when physically and chemically weathered microplastics are exposed to the oily digestive fluids conditions of fish and seabirds.

Ambient fine particulate matter (PM2.5) pollution has been implicated in the development of hypertensive disorders of pregnancy. However, evidence on the effects of PM2.5-derived chemical constituents on gestational blood pressure (BP) is limited, and the potential mechanisms underlying the association remain unclear. In this study, we repeated three consecutive 72-h personal air sampling and BP measurements in 215 pregnant women for 590 visits during pregnancy. Individual PM2.5 exposure level was assessed by gravimetric method and 28 PM2.5 chemical constituents were analyzed by ED-XRF method. Plasma biomarkers of endothelial function and inflammation were measured using multiplexed immunoassays. Robust multiple linear regression models were used to estimate the associations among personal PM2.5 exposure and chemical constituents, BP changes (compared with pre-pregnancy BP) and plasma biomarkers. Mediation analyses were performed to evaluate underlying potential pathways. Result showed that exposure to PM2.5 was significantly associated with increases in systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) in the early second trimester. Meanwhile, elevated concentration of lead (Pb) constituent in PM2.5 was significant associated with increases in DBP and MAP after adjusting for PM2.5 total mass. PM2.5 and Pb constituent also presented positive associations with plasma biomarkers of endothelial function (ET-1, E-selectin, ICAM-1) and inflammation (IL-1β, IL-6, TNFα) significantly. After multiple adjustment, elevated ET-1 and IL-6 were significantly correlated with increased gestational BP, and respectively mediated 1.24%–25.06% and 7.01%–10.69% of the increased BP due to PM2.5 and Pb constituent exposure. In conclusion, our results suggested that personal exposure to PM2.5 and Pb constituent were significantly associated with increased BP during pregnancy, and the early second trimester might be the sensitive window of PM2.5 exposure. The endothelial dysfunction and elevated inflammation partially mediated the effect of PM2.5 and Pb constituent on BP during pregnancy.