A total of 138 samples including urban soil, surface dust, atmospheric dustfall, and commercial food were collected from the semi-arid industrial city of Lanzhou in Northwest China, and 22 phthalate esters (PAEs) were analyzed in these samples by gas chromatography-mass spectrometry for the pollution characteristics, potential sources, and combined exposure risks of PAEs. The results showed that the total concentration of 22 PAEs (Sigma(22)PAEs) presented surface dust (4.94 x 10(4) ng/g) >> dustfall (1.56 x 10(4) ng/g) >> food (2.14 x 10(3) ng/g) >> urban soil (533 ng/g). Di-n-butyl phthalate (DNBP), di-isobutyl phthalate, di(2-ethylhexyl) phthalate (DEHP), and di-isononyl phthalate/di-isodecyl phthalate were predominant in the environmental media and commercial food, being controlled by priority (52.1%-65.5%) and non-priority (62.1%) PAEs, respectively. Elevated Sigma(22)PAEs in the urban soil and surface dust was found in the west, middle, and east of Lanzhou. Principal component analysis indicated that PAEs the urban soil and surface dust were related with the emissions of products containing PAEs, atmosphere depositions, and traffic and industrial emissions. PAEs in the foods were associated with the growth and processing environment. The health risk assessment of United States Environmental Protection Agency based on the Chinese population exposure parameters indicated that the total exposure dose of 22 PAEs was from 0.111 to 0.226 mg/kg/day, which were above the reference dose (0.02 mg/kg/day) and tolerable daily intake (TDI, 0.05 mg/kg/day) for DEHP (0.0333-0.0631 mg/kg/day), and TDI (0.01 mg/kg/day) for DNBP (0.0213-0.0405 mg/kg/day), implying that the exposure of PAEs via multi-media should not be ignored; the total non-carcinogenic risk of six priority PAEs was below 1 for the three environmental media (1.21 x 10(-5)-2.90 x 10(-3)), while close to 1 for food (4.74 x 10(-1)-8.76 x 10(-1)), suggesting a potential non-carcinogenic risk of human exposure to PAEs in food; the total carcinogenic risk of BBP and DEHP was below 1 x 10(-6) for the three environmental media (9.13 x 10(-10)-5.72 x 10(-7)), while above 1 x 10(-4) for DEHP in food (1.02 x 10(-4)), suggesting a significantly carcinogenic risk of human exposure to DEHP in food. The current research results can provide certain supports for pollution and risk prevention of PAEs.

Pentachlorophenol (PCP) - cadmium (Cd) complex pollution has been identified as a form of persistent soil pollution in south China, exerting detrimental impacts on the indigenous soil bacterial communities. Hence, it is worthwhile to investigate whether and how bacterial populations alter in response to these pollutants. In this study, Escherichia coli was used as a model bacterium. Results showed that PCP exposure caused bacterial cell membrane permeability changes, intracellular ROS elevation, and DNA fragmentation, and triggered apoptosislike cell death at low exposure concentration and necrosis at high exposure concentration. Cd exposure caused severe oxidative damage and cell necrosis in the tested bacterial strain. The co-exposure to PCP and Cd elevated the ROS level, stimulated the bacterial caspase activity, and induced DNA fragmentation, thereby leading to an apoptosis-like cell death. In conclusion, PCP-Cd complex pollution can cause bacterial population to decrease through apoptosis-like cell death pathway. However, it is worth noting that the subpopulation survives under the complex pollution stress.