Population level risk assessment: practical considerations for evaluation of population models from a risk assessor's perspective

Population models are increasingly being considered as a tool for pesticide risk assessment in order to evaluate how potential effects act on the population level and population recovery. While the importance and difficulties of such models have been discussed by various authors during the past decade, mainly with a focus on how to describe or develop such models, several biological and methodological aspects have never been addressed so far, which are relevant for the application of models in risk assessment. These include a critical review of our knowledge of a species, the use of field data by taking methodological constraints into account, how to include uncertainty in model validation or how to measure effects. Although these aspects will be critical for the acceptance of population models by authorities, most of them apply not only to population models, but also to standard risk assessment. In the present article, we give practical recommendations for addressing these questions in population level risk assessments.     

Objectively best or most acceptable? Expert and lay knowledge in Swedish wind power permit processes

This article analyses legal aspects of the Swedish wind power development, theoretically based on how different types of knowledge are represented in legal contexts, mainly in the courts. A sample of appealed wind power permits is analysed, a handful of relevant informants are interviewed – including two judges in the Land and Environment Court and the appeal court – and the legal setting is analysed. Of key interest here is the interplay between expert and lay statements in the court cases, which here is related to the concepts of calculating and communicative rationalities that are developed in the planning literature. The results indicate that the juridification – which takes place as a permit issue is appealed in the judiciary system – supports the calculating rationality more than the communicative, and that the plaintiffs often attempt to adapt in how they shape their argumentation.     

波罗的海鱼类和甲壳类的毒性物质及繁殖失调

在波罗的海生态系统中,由于毒性物质(例如DDT,PCB)的生物积累作用,在食物链上层捕食者(如海豹和食鱼鸟类)中已出现了繁殖失调.在过去25年间繁殖失调还影响到鱼类.然而,还没有强有力的证据说明这些问题是有毒物质引起的.更确切地说,这种失调似乎是由两种以上生物或生物的因素共同引起的.杀死鲑鱼和鳟鱼幼体的M74综合症,是由于缺乏硫胺素(维生素B1).许多因素可以导致维生素B1缺乏,包括鲑鱼的食物和卤代有机化合物.鳕鱼不生M74病,其资源得不到恢复是由于繁殖区域溶解氧缺乏和过度捕捞.肉类加工厂排放物中的毒性物质,而不是机械作用和活性物质,抑制了生殖腺的发育.肉类加工厂所在海域的外侧鱼类资源缺乏可以解释为幼鱼缺乏食物,而不是繁殖失败.有关波罗的海甲壳类繁殖失调的资料很少.大部分资料都是关于端足类Monoporeoaaffnis的研究,该种生物已被用于监测计划.该种生物的繁殖失调现象例如胚胎畸形、死亡,以及雌雄性不同时成熟等已有报道.     

持久性有机污染物(POPs)的监测:来自瑞典韦特恩湖的例子

位于瑞典南部的韦特恩湖是一个大的贫营养化湖泊,它具有高的水面与流域面积比率(大约为0.4)和60年的驻水时间.此湖结合了对大气POP污染的敏感性、对POPs影响的普通敏感性和较慢的浓度降低.提出了鱼体内PCBs和DDT从20世纪60年代一直到1996年的时间系列,以及韦特恩湖沉积物中TCDD的数据,并和其它大湖泊进行了比较.有关北极红点鲑(Salvelinus salvelinus)体内POPs的长期数据集显示每年PCBs有大约5%,DDT有13%的减少.这些速度和其它研究相一致.也讨论了营养物质及其生物效应,以及影响具有长驻水时间的贫营养化湖泊命运的因素.我们提出贫营养的干净湖泊是对于监测生物区中POPs的重要生态系统.     

Vegetation phenology gradients along the west and east coasts of Greenland from 2001 to 2015

The objective of this paper is to characterize the spatiotemporal variations of vegetation phenology along latitudinal and altitudinal gradients in Greenland, and to examine local and regional climatic drivers. Time-series from the Moderate Resolution Imaging Spectroradiometer (MODIS) were analyzed to obtain various phenological metrics for the period 2001–2015. MODIS-derived land surface temperatures were corrected for the sampling biases caused by cloud cover. Results indicate significant differences between West and East Greenland, in terms of both observed phenology during the study period, as well as the climatic response. The date of the start of season (SOS) was significantly earlier (24 days), length of season longer (25 days), and time-integrated NDVI higher in West Greenland. The sea ice concentration during May was found to have a significant effect on the date of the SOS only in West Greenland, with the strongest linkage detected in mid-western parts of Greenland.     

Animals need not be killed to reveal their body-burdens of chlorinated hydrocarbons

The levels of persistent, lipophilic pollutants in different organs and body-fluids of birds are governed by partitioning, i.e. the levels are correlated. This implies that it may be possible to estimate the total body-burden of chlorinated hydrocarbons, without sacrificing the animals, by examining the levels in secretory fluid. This hypothesis was tested on the goosander, a fish-eating waterfowl. We found that levels of PCB and DDE in secretions from the uropyginal gland were linearly related to levels in the breast muscle. Thus, by estimating the amounts of persistent pollutants in water-repellent secretions, the total body-burden could be calculated.     

An oxygenated metabolite of benzo[a]pyrene increases hepatic β-oxidation of fatty acids in chick embryos

Polycyclic aromatic hydrocarbons (PAHs) are well-known carcinogens to humans and ecotoxicological effects have been shown in several studies. However, PAHs can also be oxidized into more water soluble-oxygenated metabolites (Oxy-PAHs). The first purpose of the present project was to (1) assess the effects of a mixture containing three parent PAHs: anthracene, benz[a]anthracene, and benzo[a]pyrene versus a mixture of their oxygenated metabolites, namely: anthracene-9,10-dione, benz[a]anthracene-7,12-dione, and 9,10-dihydrobenzo[a]pyrene-7-(8H)-one on the hepatic fatty acid β-oxidation in chicken embryos (Gallus gallus domesticus) exposed in ovo. The second and also main purpose of the project was to (2) assess the effects of the parent PAHs versus their oxy-PAHs analogues when injected individually, followed by (3) additional testing of the individual oxy-PAHs. The hepatic β-oxidation was measured using a tritium release assay with [9,10-³H]-palmitic acid (16:0) as substrate. The result from the first part (1) showed reduced hepatic β-oxidation after exposure in ovo to a mixture of three PAHs, however, increased after exposure to the mixture of three oxy-PAHs compared to control. The result from the second part (2) and also the follow-up experiment (3) showed that 9,10-dihydrobenzo[a]pyrene-7-(8H)-one was the causative oxy-PAH. The implication of this finding on the risk assessment of PAH metabolite exposure in avian wildlife remains to be determined. To the best of our knowledge, no similar studies have been reported.