Average concentrations of PM_<b>2.5</b>, PM_<b>10</b> and TSP in the present study and those from previous studies (μg/m^<b>3</b>).

<p>ETS, represents environmental tobacco smoking.</p><p>Average concentrations of PM_<b>2.5</b>, PM_<b>10</b> and TSP in the present study and those from previous studies (μg/m^<b>3</b>).</p

Polybrominated Diphenyl Ethers (PBDEs) in PM_2.5, PM₁₀, TSP and Gas Phase in Office Environment in Shanghai, China: Occurrence and Human Exposure

<div><p>To evaluate risk via inhalation exposure of polybrominated diphenyl ethers (PBDEs) in office environment, thirty-six pairs air samples including PM_2.5 (particles with aerodynamic diameter less than 2.5 μm), PM₁₀ (particles with aerodynamic diameter less than 10 μm), total suspended particles (TSP) with matching gas phase were collected in office environment in Shanghai, China. The average concentrations of PM_2.5, PM₁₀ and TSP were 20.4, 27.2 and 50.3 μg/m₃, respectively. Σ₁₅PBDEs mean concentrations in PM_2.5, PM₁₀, TSP and gas phase were 51.8, 110.7, 148 and 59.6 pg/m³, respectively. Much more PBDEs distributed in fine fractions than coarse ones. PBDEs congener profiles found in PM_2.5, PM₁₀ and TSP (dominated by BDE-209) were different from that in gas phase (dominated by the tri- to penta-BDEs). Approximately 3.20 pg/kg/d PM_2.5 bound PBDEs can be inhaled into the lung; 3.62 pg/kg/d PM₁₀-PM_2.5(particles with aerodynamic diameter of 2.5-10 μm) bound PBDEs tended to be deposited in the upper part of respiratory system, and the intake of PBDEs via gas-phase was 2.74 pg/kg/d. The exposure of PBDEs was far below the minimal risk levels (MRLs), indicating lower risk from PBDEs via inhalation in the studied office in Shanghai.</p></div

Health risks of inhalation PBDEs exposure via PM_2.5, PM₁₀, TSP and gas phase.

<p>Health risks of inhalation PBDEs exposure via PM_2.5, PM₁₀, TSP and gas phase.</p

Daily exposure to PBDEs via inhalation of PM_2.5, PM₁₀, TSP and gas phase.

<p>Daily exposure to PBDEs via inhalation of PM_2.5, PM₁₀, TSP and gas phase.</p

Concentrations of PBDEs congeners in PM_2.5, PM₁₀, TSP and gas phase (Summer: June, July and August 2012; Winter: December 2012, January, and February 2013).

<p>Concentrations of PBDEs congeners in PM_2.5, PM₁₀, TSP and gas phase (Summer: June, July and August 2012; Winter: December 2012, January, and February 2013).</p

Exposures of BDEs of PM-bound and gas-phase via inhalation (pg/kg/d).

<p>Exposures of BDEs of PM-bound and gas-phase via inhalation (pg/kg/d).</p

Organic Contaminants in Chinese Sewage Sludge: A Meta-Analysis of the Literature of the Past 30 Years

The production of sewage sludge is increasing in China but with unsafe disposal practices, causing potential risk to human health and the environment. Using literature from the past 30 years (<i>N</i> = 159), we conducted a meta-analysis of organic contaminants (OCs) in Chinese sludge. Most data were available from developed and populated regions, and no data were found for Tibet. Since 1987, 35 classes of chemicals consisting of 749 individual compounds and 1 mixture have been analyzed, in which antibiotics and polycyclic aromatic hydrocarbons (PAHs) were the most targeted analytes. For 13 classes of principal OCs (defined as chemicals detected in over five studies) in sludge, the median (expressed in nanograms per gram dry weight) was the highest for phthalate esters (27 900), followed by alkylphenol polyethoxylates (12 000), synthetic musks (5800), antibiotics (4240), PAHs (3490), ultraviolet stabilizers (670), bisphenol analogs (160), organochlorine pesticides (110), polybrominated diphenyl ethers (100), pharmaceuticals (84), hormones (69), perfluorinated compounds (21), and polychlorinated biphenyls (15). Concentrations of PAHs in sludges collected between 1998 and 2012 showed a decreasing trend. Study findings suggest the need for a Chinese national sewage sludge survey to identify and regulate toxic OCs, ideally employing both targeted as well as nontargeted screening approaches

Frequency distribution of MEHP levels in cord blood and meconium.

<p> The frequency distribution of MEHP levels in cord blood and meconium, illustrating that MEHP levels in meconium were much higher than those in cord blood.</p

Regression analysis between non-POPs levels in maternal and cord blood.

<p> Regression analysis was used to analyze the relationship between these EDs levels in maternal and cord blood. (A) The relationship between MEHP levels in maternal and cord blood. The regression coefficient was 0.807, meaning that about 80% MEHP could cross the placenta; (B) The relationship between OP levels in maternal and cord blood. The regression coefficient was 0.846, meaning that about 85% OP could go through the placenta; (C) The relationship between 4-NP levels in maternal and cord blood. The regression coefficient was 0.862, meaning that more than 86% 4-NP could cross the placenta.</p

Endocrine disruptor levels in specimens (mg/L).

<p>Endocrine disruptor levels in specimens (mg/L).</p