This review summarizes our current state of knowledge regarding the potential biological effects of mercury (Hg) exposure on fish and wildlife in the Canadian Arctic. Although Hg in most freshwater fish from northern Canada was not sufficiently elevated to be of concern, a few lakes in the Northwest Territories and Nunavut contained fish of certain species (e.g. northern pike, Arctic char) whose muscle Hg concentrations exceeded an estimated threshold range (0.5-1.0 µg g(-1) wet weight) within which adverse biological effects begin to occur. Marine fish species generally had substantially lower Hg concentrations than freshwater fish; but the Greenland shark, a long-lived predatory species, had mean muscle Hg concentrations exceeding the threshold range for possible effects on health or reproduction. An examination of recent egg Hg concentrations for marine birds from the Canadian Arctic indicated that mean Hg concentration in ivory gulls from Seymour Island fell within the threshold range associated with adverse effects on reproduction in birds. Mercury concentrations in brain tissue of beluga whales and polar bears were generally lower than levels associated with neurotoxicity in mammals, but were sometimes high enough to cause subtle neurochemical changes that can precede overt neurotoxicity. Harbour seals from western Hudson Bay had elevated mean liver Hg concentrations along with comparatively high muscle Hg concentrations indicating potential health effects from methylmercury (MeHg) exposure on this subpopulation. Because current information is generally insufficient to determine with confidence whether Hg exposure is impacting the health of specific fish or wildlife populations in the Canadian Arctic, biological effects studies should comprise a major focus of future Hg research in the Canadian Arctic. Additionally, studies on cellular interactions between Hg and selenium (Se) are required to better account for potential protective effects of Se on Hg toxicity, especially in large predatory Arctic fish, birds, and mammals.
The legislative basis of the federal Canadian government's control of toxic chemicals is described and examples are given of the practical application, ranging from recommendations to a ban on the sale of the product. The ordered sequence of risk assessment and the application of risk estimation techniques are considered. It is clear that the ultimate political decision is not amenable to simplistic scientific analysis, although risk analysis is valuable in defining, rather than solving, the problem.
Considerable variations in the frequency of spontaneous chromosomal aberrations were revealed during a cytogenetic study of two groups of adolescents from ecologically different areas of Kemerovskaya oblast'. In a sample of adolescents living in an industrial center (the Kemerovo city), this parameter (1.4 +/- 0.37%) did not exceed the population average value, whereas adolescents of the same age from a mountain region with sparse industry (the town of Tashtagol) exhibited, on average, a frequency of 5.87 +/- 0.62%. An increased proportion of chromosomal-type aberrations in the qualitative spectrum of cytogenetic damage, which was observed for the group of adolescents from Tashtagol, suggests that this population was exposed to radiation.
Regulatory agencies require numbers to provide health protection. The manner in which these numbers are derived from animal experiments and human epidemiology is considered together with the limitations and inadequacies of these numbers. Some recent examples of risk assessment in Canada are given including asbestos, drinking water, and indoor air quality. The value of these numbers in providing a measure of the hazard in a wider perspective is stressed, although they can never be the sole determinant of public policy.
BACKGROUND: Bone toxicity has been linked to organochlorine exposure following a few notable poisoning incidents, but epidemiologic studies in populations with environmental organochlorine exposure have yielded inconsistent results. OBJECTIVES: The aim of this study was to investigate whether organochlorine exposure was associated with bone mineral density (BMD) in a population 60-81 years of age (154 males, 167 females) living near the Baltic coast, close to a river contaminated by polychlorinated biphenyls (PCBs). METHODS: We measured forearm BMD in participants using dual energy X-ray absorptiometry; and we assessed low BMD using age- and sex-standardized Z-scores. We analyzed blood samples for five dioxin-like PCBs, the three most abundant non-dioxin-like PCBs, and p,p'-dichloro-phenyldichloroethylene (p,p'-DDE). RESULTS: In males, dioxin-like chlorobiphenyl (CB)-118 was negatively associated with BMD; the odds ratio for low BMD (Z-score less than -1) was 1.06 (95% confidence interval, 1.01-1.12) per 10 pg/mL CB-118. The sum of the three most abundant non-dioxin-like PCBs was positively associated with BMD, but not with a decreased risk of low BMD. In females, CB-118 was positively associated with BMD, but this congener did not influence the risk of low BMD in women. CONCLUSIONS: Environmental organochlorine exposures experienced by this population sample since the 1930s in Sweden may have been sufficient to result in sex-specific changes in BMD.
Life cycle impact assessment (LCIA) and comparative risk assessment (RA) use the same building blocks for analyzing fate and potential effects of toxic substances. It is tacitly assumed that emission-effect calculations can give uniform and decisive answers in debates on toxicity problems. For several decades, mainstream policy sciences have taken a different starting point when analyzing decision making on complex, controversial societal issues. Such controversies in essence are thought to be caused by the fact that different actor coalitions adhere to a different, but in scientific terms equally reasonable, conceptualization or "framing" of the problem. A historical, argumentative analysis of the Dutch chlorine debate and the Swedish PVC debate shows that this is also true in the discussions on toxic substances. Three frames have been identified, which were coined the "risk assessment frame," "the strict control frame," and the "precautionary frame." These frames tacitly disagree about the extent of knowledge/ignorance about the impacts of substances, the robustness/fallibility of emission-reduction schemes, and the robustness/vulnerability of nature. The latter frame, adhered to by environmentalists, seeks to judge substances mainly on their inherent safety. Under the current institutional arrangements and practices, RA and LCIA are executed mainly in line with the philosophy expressed by the risk assessment frame. This article gives various suggestions for dealing with framing in debates on toxic substances. One of the options is elaborated in somewhat more detail, i.e., the development of multiple indicators and calculation schemes for RA and LCIA that reflect the different frames. An outline is given for a possible indicator system reflecting the precautionary principle.
Biomonitoring survey conducted with glaucous gulls from Svalbard have demonstrated that this top-predator-scavenger species accumulates a wide array of chemicals of environmental concern, including organohalogens, trace elements, organometals, and several non-halogenated and non-metallic-compounds. Among these contaminants are those subjected to global bans or restrictions in North America and Europe (e.g., legacy OC's, penta-, and octa-PBDE technical mixtures and mercury). In addition, some currently produced chemicals were found in gulls that lack and global use regulation (e.g., deca-PBDE , HBCD, and other non-PBDE BFR additives, siloxanes, and selected PFASs). Svalbard glaucous gulls are also exposed to contaminant metabolites that, at time, are more bioactive than their precursors (e.g., oxychlordane, p,p'-DDE, OH- and MeSo2-PCBs, and OH-PBDEs) Concentrations of legacy OCs (PCBs, DDTs, CHLs, CBzs, dieldrin, PCDD/Fs, and mirec) in tissues, blood, and eggs of Svalbard glaucous gulls have displayed the highest contamination levels among glaucous gull populations that inhabit Greenland (Cleemann et al. 2000) Jan Mayen (Gabrielsen et al. 1997), Alaska (Vander Pol et al. 2009), and the Canadian Arctic (Braune et a. 2005). To date, measurements obtaines on more novel organohalogens (e.g., OH- and MeSo2-containing metabolites, BFRs and PFASs) in Svalbard glaucous gull samples generally confirm that the spatial and trophodynamic trends of the legacy OC concentrations, whereas no clear trend emerges from surveys of trace elements and organometals. Using the glaucous gull as biosentinel species provides clear evidence that Svalbard and the European Arctic environment is exposed to a complex mixture of legacy and more recently introduced PBT-like substances.
The ecological footprint method has been successful in communicating environmental impacts of anthropogenic activities in the context of ecological limits. We introduce a chemical footprint method that expresses ecotoxicity impacts from anthropogenic chemical emissions as the dilution needed to avoid freshwater ecosystem damage. The indicator is based on USEtox characterization factors with a modified toxicity reference point. Chemical footprint results can be compared to the actual dilution capacity within the geographic vicinity receiving the emissions to estimate whether its ecological limit has been exceeded and hence whether emissions can be expected to be environmentally sustainable. The footprint method was illustrated using two case studies. The first was all inventoried emissions from European countries and selected metropolitan areas in 2004, which indicated that the dilution capacity was likely exceeded for most European countries and all landlocked metropolitan areas. The second case study indicated that peak application of pesticides alone was likely to exceed Denmark's freshwater dilution capacity in 1999-2011. The uncertainty assessment showed that better spatially differentiated fate factors would be useful and pointed out other major sources of uncertainty and some opportunities to reduce these.