Does remediation save lives? On the cost of cleaning up arsenic-contaminated sites in Sweden

Swedish environmental policy is based on 16 environmental quality objectives (Gov. Bill 2000/01:130 and Gov.Bill 2004/05:150).1 One of the most challenging objectives,‘A non toxic environment’, has two interim targets that concern remediation of contaminated sites. In sum, they state that the highest priority should be given to sites posing the highest risks to human health and the environment.2 By eliminating pollutants in soil, groundwater and sediment, the interim targets aim to reduce risks to human health and the environment. In Sweden, 83,000 sites are potentially contaminated due to previous industrial activities. According to the Swedish Environmental Protection Agency (EPA), the administrator of the governmental funds for remediation, approximately 1500 of these sites contain contaminant concentrations that could seriously harm human health and the environment (Swedish EPA, 2008a). To reach the interim targets, all these sites need to be remediated by 2050. Remediation of contaminated sites has so far cost more than SEK 3,000 million.3 The approximated cost to mitigate the potential risks at the most harmful sites is estimated at SEK 60,000 million.4 The Swedish government’s funding for remediation presently comes in the form of a directed grant (sakanslag). The directed grant, administrated by the Swedish EPA, subsidises remediation of contaminated sites that were contaminated prior to modern environmental legislation (in 1969) or for which no liable party can be found. The directed grant amounts to approximately 455 millions annually, which corresponds to about 10 percent of the annual national funds for environmental protection (Gov. Bill 2007/08:1). To make it possible to prioritise among contaminated sites, the Swedish EPA has developed a method for risk assessment called the ‘MIFO’ (i.e. the Method for Inventory of Contaminated Sites). The risk assessment does not take into account the actual exposure at a contaminated site. Risk is instead assessed based on divergence from guideline values for acceptable concentrations given a standardised (i.e. worst case) exposure situation on an individual level. This means that a site can be remediated without any individuals actually being exposed. The expected risk reduction is consequently not quantified. This eliminates the possibility of valuing the risk reduction, which should be weighed against the remediation cost. The purpose of this paper is to analyse how health effects, in the form of cancer risks, from sites contaminated by arsenic are valued implicitly in remediation. By using an environmental medicine approach that takes exposure into account, and without underestimating the potential health consequences of arsenic exposure, our purpose is to place arsenic risk management in the overall picture of live-saving interventions. In the case of cancer prevention, it is necessary to recognise that focus on an environmental carcinogen like arsenic may draw public attention – and funding – away from mental health risks like ambient air pollution and indoor radon. Although environmental pollution accounts for less than ten percent of all cancer cases (Harvard Centre for Cancer Prevention, 1996; Saracci and Vineis, 2007), environmental factors are important to recognize since they may be preventable. We emphasise, however, the inefficiency in becoming overly concerned about small risks while, at the same time, losing sight of the large risks. If society’s spending on lifesaving measures with small effects (i.e. a small number of lives saved) crowds out spending on lifesaving measures with large effects, then remediation can, in fact, even be said to waste lives. By using data on 23 arsenic-contaminated sites in Sweden, we estimate the sitespecific cancer risks and calculate the cost per life saved by using the sites’ remediation costs. Our results show that the cost per life saved through remediation is much higher than that associated with other primary prevention measures, indicating that the ambition level of Swedish remediation may be too high.

Extremvärme ett ökande problem för globala folkhälsan : Klimatförändringarnas negativa hälsoeffekter drabbar även Sverige

High temperatures have a direct impact on body functions. Heat waves increase mortality risks due to myocardial infarction, stroke, and pulmonary disease. Cold temperatures also increase mortality, but with a longer latency. A recent study found only a small difference between the minimal mortality temperature (MMT) and the temperatures at which mortality rose steeply, although the majority of deaths occurred at temperatures below MMT. Global climate change with increasing temperatures seriously threatens health, work capacity, and generation of household incomes, particularly among poor people in hot countries. In Sweden, heat waves increase mortality in vulnerable groups of elderly people and patients with chronic heart and lung diseases, as well as those performing intensive physical work in hot environments. The medical profession can play an important role not only in prevention of climate change, but also in adaptation to climate change with the goal of minimizing health risks

Regulated mitochondrial DNA replication during oocyte maturation is essential for successful porcine embryonic development.

Cellular ATP is mainly generated through mitochondrial oxidative phosphorylation, which is dependent on mitochondrial DNA (mtDNA). We have previously demonstrated the importance of oocyte mtDNA for porcine and human fertilization. However, the role of nuclear-encoded mitochondrial replication factors during oocyte and embryo development is not yet understood. We have analyzed two key factors, mitochondrial transcription factor A (TFAM) and polymerase gamma (POLG), to determine their role in oocyte and early embryo development. Competent and incompetent oocytes, as determined by brilliant cresyl blue (BCB) dye, were assessed intermittently during the maturation process for TFAM and POLG mRNA using real-time RT-PCR, for TFAM and POLG protein using immunocytochemistry, and for mtDNA copy number using real-time PCR. Analysis was also carried out following treatment of maturing oocytes with the mtDNA replication inhibitor, 2',3'-dideoxycytidine (ddC). Following in vitro fertilization, preimplantation embryos were also analyzed. Despite increased levels of TFAM and POLG mRNA and protein at the four-cell stage, no increase in mtDNA copy number was observed in early preimplantation development. To compensate for this, mtDNA appeared to be replicated during oocyte maturation. However, significant differences in nuclear-encoded regulatory protein expression were observed between BCB(+) and BCB(-) oocytes and between untreated oocytes and those treated with ddC. These changes resulted in delayed mtDNA replication, which correlated to reduced fertilization and embryonic development. We therefore conclude that adherence to the regulation of the timing of mtDNA replication during oocyte maturation is essential for successful embryonic development

Risks for human and animal health related to the presence of phorbol esters in Jatropha kernel meal

The Panel wishes to thank the members of the Working Group on Phorbol Esters: Bruce Cottrill, Stefano Dall'Acqua, Johanna Fink-Gremmels, Harinder P.S. Makkar and Manfred Metzler for the preparatory work on this scientific opinion, and EFSA staff: Marco Binaglia, Karen Mackay and Rositsa Serafimova for the support provided to this scientific opinion.Peer reviewedPublisher PD

Acute health risks related to the presence of cyanogenic glycosides in raw apricot kernels and products derived from raw apricot kernels

Peer reviewedPublisher PD

Presence of microplastics and nanoplastics in food, with particular focus on seafood

The Panel wishes to thank the members of the Working Group on the presence of microplastics and nanoplastics in food, with particular focus on seafood: Francesco Cubadda, Christer Hogstrand, Peter Hollman, Hendrik Van Loveren, Anne-Katrine Lundebye and Annette Petersen for the preparatory work on this statement, the hearing expert: Stephanie Wright and EFSA staff member: Karen Mackay for the support provided to this statement.Peer reviewedPublisher PD

Risk for animal and human health related to the presence of dioxins and dioxin-like PCBs in feed and food

The European Commission asked EFSA for a scientific opinion on the risks for animal and human health related to the presence of dioxins (PCDD/Fs) and DL-PCBs in feed and food. The data from experimental animal and epidemiological studies were reviewed and it was decided to base the human risk assessment on effects observed in humans and to use animal data as supportive evidence. The critical effect was on semen quality, following pre- and postnatal exposure. The critical study showed a NOAEL of 7.0 pg WHO2005-TEQ/g fat in blood sampled at age 9 years based on PCDD/F-TEQs. No association was observed when including DL-PCB-TEQs. Using toxicokinetic modelling and taking into account the exposure from breastfeeding and a twofold higher intake during childhood, it was estimated that daily exposure in adolescents and adults should be below 0.25 pg TEQ/kg bw/day. The CONTAM Panel established a TWI of 2 pg TEQ/kg bw/week. With occurrence and consumption data from European countries, the mean and P95 intake of total TEQ by Adolescents, Adults, Elderly and Very Elderly varied between, respectively, 2.1 to 10.5, and 5.3 to 30.4 pg TEQ/kg bw/week, implying a considerable exceedance of the TWI. Toddlers and Other Children showed a higher exposure than older age groups, but this was accounted for when deriving the TWI. Exposure to PCDD/F-TEQ only was on average 2.4- and 2.7-fold lower for mean and P95 exposure than for total TEQ. PCDD/Fs and DL-PCBs are transferred to milk and eggs, and accumulate in fatty tissues and liver. Transfer rates and bioconcentration factors were identified for various species. The CONTAM Panel was not able to identify reference values in most farm and companion animals with the exception of NOAELs for mink, chicken and some fish species. The estimated exposure from feed for these species does not imply a risk.Peer reviewe