Next to imposing direct lethal effects, pollutants may also indirectly impose mortality by making prey organisms more vulnerable to predation. We report that four water boatmen species differed strongly in direct endosulfan-imposed mortality, and only the species that suffered highest mortality, Sigara iactans, also showed a reduction in escape swimming speed. While head AChE activity was inhibited in all four species, body ChE was only inhibited in S. iactans where it covaried with escape swimming speed, indicating a mechanistic link between body ChE and swimming speed. Our study underscores the need for risk assessment to consider sublethal pollutant effects, which may considerably affect survival rates under natural conditions, also when testing concentrations of a pesticide that cause direct mortality. Such sublethal effects may generate discrepancies between laboratory and field studies and should be considered when designing safety factors for toxicants where the risk assessment is solely based on LC50 values.

Pre-requisite for reliable O₃ risk assessment for plants is determination of stomatal O₃ uptake. One unaddressed uncertainty in this context relates to transpiration-induced molecular collisions impeding stomatal O₃ influx. This study quantifies, through physical modelling, the error made when estimating stomatal O₃ flux without accounting for molecular collisions arising from transpiratory mass flow of gas out of the leaf. The analysis demonstrates that the error increases with increasing leaf-to-air water vapour mole fraction difference (Δw), being zero in water vapour saturated air and 4.2% overestimation at Δw of 0.05. Overestimation is approximately twice as large in empirical studies quantifying stomatal O₃ flux from measured leaf or canopy water flux, if neglecting both water vapour-dry air collisions (causing overestimation of leaf conductance) and collisions involving O₃. Correction for transpiration-induced molecular collisions is thus relevant for both empirical research and for large-scale modelling of stomatal O₃ flux across strong spatial Δw gradients.

Adsorption of mercury (Hg) on lignin was studied at a range of pH values using a combination of batch adsorption experiments, a surface complexation model (SCM) and synchrotron X-ray absorption spectroscopy (XAS). Surface complexation modeling indicates that three types of acid sites on lignin surfaces, namely aliphatic carboxylic-, aromatic carboxylic- and phenolic-type surface groups, contributed to Hg(II) adsorption. The bond distance and coordination number of Hg(II) adsorption samples at pH 3.0, 4.0 and 5.5 were obtained from extended X-ray absorption fine structure (EXAFS) spectroscopy analysis. The results of SCM and XAS combined reveal that the predominant adsorption species of Hg(II) on lignin changes from HgCl₂ ⁰ to monodentate complex –C–O–HgCl and then bidentate complex –C–O–Hg–O–C– with increasing pH value from 2.0 to 6.0. The good agreement between SCM and XAS results provides new insight into understanding the mechanisms of Hg(II) adsorption on lignin.

Polyethylene passive samplers (PE) were deployed in Narragansett Bay, RI, to examine freely dissolved concentrations of polybrominated diphenyl ethers (PBDEs) in surface, bottom, and sediment porewater. PBDE congeners in the water column and porewater were below 3 pg L⁻¹. In the surface water, only PBDE congeners containing up to 5 bromines were detected, while in the deeper water congeners 153 and 154 (6 bromines) were also detected. Activity ratios of surface-bottom water and porewater-bottom water suggested that lower brominated (di-tetra) congeners reached Narragansett Bay from surface waters and sediments. PBDEs in the surface water probably originated from a combination of air–water exchange, freshwater runoff, rivers, and wastewater treatment plants. It is suggested that deep water was the source of higher brominated PBDEs to the Bay implying that the more hydrophobic PBDEs reached depth on particles and/or that these congeners were degraded in sediments. On-going sources supply PBDEs to Narragansett Bay.

Polycyclic aromatic hydrocarbon (PAH) diagnostic ratios have recently come into common use as a tool for identifying and assessing pollution emission sources. Some diagnostic ratios are based on parent PAHs, others on the proportions of alkyl-substituted to non-substituted molecules. The ratios are applicable to PAHs determined in different environmental media: air (gas + particle phase), water, sediment, soil, as well as biomonitor organisms such as leaves or coniferous needles, and mussels. These ratios distinguish PAH pollution originating from petroleum products, petroleum combustion and biomass or coal burning. The compounds involved in each ratio have the same molar mass, so it is assumed they have similar physicochemical properties. Numerous studies show that diagnostic ratios change in value to different extents during phase transfers and environmental degradation. The paper reviews applications of diagnostic ratios, comments on their use and specifies their limitations.

Air samples were collected at different sites in and around two wastewater treatment plants (WWTPs) located in central Italy to determine the concentrations, compositional profiles and contribution to ambient levels of eight polybrominated diphenyl ethers (PBDEs). The investigated WWTPs were selected as they treat industrial wastewater produced by local textile industries along with municipal wastewater. PBDE concentrations within the WWTPs were higher than those measured at reference sites located 4 and 5km away with BDE-209 dominating the BDE congener composition in all air samples in 2008. Ambient PBDE concentrations measured in and around the WWTPs and estimates of emissions from aeration tanks suggest that WWTPs are sources of PBDEs to ambient air. Principal component analysis and Pearson correlations confirmed this result. The effect of distance from the plant and wind direction on atmospheric concentrations was also investigated. Although the primary fate of PBDEs in WWTPs will be partitioning to sewage sludge, this study suggests that plants can provide a measurable source of these compounds to local ambient air.

This study was designed to biomonitor the effect of PAH extracts from urban areas on the DNA of lung cell cultures. The analyses of the polycyclic aromatic hydrocarbons (PAHs) were performed in atmospheric PM₂.₅ and PM₁₀ collected at three sampling sites with heavy traffic located in the Metropolitan Area of Porto Alegre (MAPA) (Brazil). The concentrations of 16 major PAHs were determined according to EPA. Comet assay on V79 hamster lung cells was chosen for genotoxicity evaluation. Temperature, humidity, and wind speed were recorded. With regard to the damage index, higher levels were reported in the extract of particulate matter samples from the MAPA during the summer. High molecular weight compounds showed correlation with DNA damage frequency and their respective carcinogenicity.

The comparative accumulation of C₄–C₁₅ perfluorinated sulfonates (PFSAs) and carboxylates (PFCAs), and several precursors (e.g., perfluorooctane sulfonamide, N-methyl-FOSA, and fluorotelomer unsaturated acids and alcohols) was examined in tissues (liver, brain, muscle, and adipose), plasma/red blood cells (RBCs) and whole egg clutches (yolk and albumen) of female herring gulls collected in 2010 from Chantry Island, Lake Huron of the Laurentian Great Lakes. Highest mean ∑PFSA concentrations were in yolk, followed by adipose, liver, plasma, muscle, RBCs, and brain. Highest mean ∑PFCA concentrations were in yolk, followed by brain, plasma, liver, RBC, adipose and muscle. PFOS accounted for >88% of ∑PFSA in all samples; the liver, plasma/RBCs, muscle and adipose PFCA patterns were dominated by C₈–C₁₁ PFCAs, whereas C₁₀–C₁₅ PFCAs in brain and yolk. Among PFSAs and PFCAs there is tissue-specific accumulation, which could be due to a number of pharmacokinetic processes.

Urbanization is an important process that alters the regional and global nitrogen biogeochemistry. In this study, we test how long-term urbanization (1952–2004) affects the nitrogen flows, emissions and drivers in the Greater Shanghai Area (GSA) based on the coupled human and natural systems (CHANS) approach. Results show that: (1) total nitrogen input to the GSA increased from 57.7 to 587.9 Gg N yr⁻¹ during the period 1952–2004, mainly attributing to fossil fuel combustion (43%), Haber–Bosch nitrogen fixation (31%), and food/feed import (26%); (2) per capita nitrogen input increased from 13.5 to 45.7 kg N yr⁻¹, while per gross domestic product (GDP) nitrogen input reduced from 22.2 to 0.9 g N per Chinese Yuan, decoupling of nitrogen with GDP; (3) emissions of reactive nitrogen to the environment transformed from agriculture dominated to industry and human living dominated, especially for air pollution. This study provides decision-makers a novel view of nitrogen management.

The rapid urbanisation of many cities in south and south-east Asia has increased the demand for bricks, which are typically supplied from brick kilns in peri-urban areas. We report visible foliar damage to mango, apricot and plum trees in the vicinity of traditional Bull’s Trench brick kilns in Peshawar, Pakistan. Visible injury symptoms, hydrogen fluoride concentrations in air, and foliar fluoride concentrations were all greater in the vicinity of brick kilns than at more distant sites, indicating that fluoride emissions from brick kilns were the main cause of damage. Interviews with local farmers established the significant impact of this damage on their livelihoods. Since poorly regulated brick kilns are often found close to important peri-urban agricultural areas, we suggest that this may be a growing but unrecognised environmental problem in regions of Asia where emission control in brick kilns has not been improved.