Search

Since 1987, the World Health Organization (WHO) carried out global surveys on polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs) in human milk. This study presents a review of the three most recent surveys from 2000 to 2010, including DDT. The objective was to identify global quantitative differences and provide baseline information for 52 countries or provide time-trends for countries with previous data. Individual human milk samples were collected following a WHO-designed procedure and combined to form a national pooled sample. Here, we report global levels for PCDDs, PCDFs, PCBs and the sum of o,p'-DDT, p,p'-DDT, o,p'-DDE, p,p'-DDE, o,p'-DDD and p,p'-DDD (ΣDDTs). A concise risk-benefit evaluation related to human milk contamination with these persistent organic pollutants (POPs) was also done. Large global and regional differences were observed. Levels of PCDDs and PCDFs were highest in India and some European and African countries. PCB levels were highest in East and West Europe. The highest levels of ΣDDTs were found in less industrialized countries. A temporal downward trend for PCDDs, PCDFs and PCBs is indicated. A risk-benefit assessment indicates that human milk levels of PCDDs, PCDFs and PCBs are still significantly above those considered toxicologically safe, while ΣDDTs are below or around those considered safe. With respect to potential adverse health effects, a more dominant role of in utero exposure versus lactational exposure is indicated. If potential adverse effects are balanced against positive health aspects for (breastfed) infants, the advantages of breastfeeding far outweigh the possible disadvantages. Our observations provide a strong argument to plea for further global source-directed measures to reduce human exposure further to dioxin-like compounds.

Background Seafood toxins pose an important risk to human health, and maximum levels were imposed by regulatory authorities throughout the world. Several toxin groups are known, each one with many analogues of the major toxin. Regulatory limits are set to ensure that commercially available seafood is not contaminated with unsafe levels. Scope and approach The mouse bioassay was used to measure the toxicity in seafood extracts to determine if a sample exceeded regulatory limits. The advantage of this approach was to provide an estimation of the total toxicity in the sample. As instrumental methods of analysis advance and serve as replacements to the mouse bioassay, the challenge is translating individual toxin concentrations into toxicity to determine whether regulatory limits have been exceeded. Such analyses provide accurate quantitation of the toxin analogues, by they have widely dissimilar potencies. Thus, knowledge of the relative toxicities is required for risk assessment and determining overall toxicity. The ratios between the toxicity of the analogues and that of a reference compound within the same toxin group are termed “Toxicity Equivalency Factors” (TEFs). Key findings and conclusions In this document, the requirements for determining TEFs of toxin analogues are described, and recommendations for research to further refine TEFs are identified. The proposed TEFs herein, when applied to toxin analogue concentrations determined using analytical methods, will provide a base to determine overall toxicity, thereby protecting human health.

The differential display technique was used to identify genes whose expression was regulated by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD). Expression of a novel sequence was up-regulated in a dose-dependent fashion in liver of Sprague-Dawley male rats exposed to both chronic and acute treatment with TCDD, as measured by densito-metry of Northern blot analyses (P < 0.01). A rapid amplification of cDNA ends (RACE) procedure was used to isolate a 1.8 kb cDNA from a rat liver cDNA preparation. This cloned cDNA, called 25-Dx, was sequenced and found to encode a peptide of 223 amino acids. In control rats, the 25-Dx gene was expressed at high levels in lung and liver. A hydrophobic domain of 14 residues followed by a proline-rich domain, both located in the N-terminal region, showed 71% homology with the transmembrane domain of the precursor for the interleukin-6 receptor and a conserved consensus sequence found in the cytokine/growth factor/prolactin receptor superfamily respectively.

The current/traditional human health risk assessment paradigm is challenged by recent scientific and technical advances, and ethical demands. The current approach is considered too resource intensive, is not always reliable, can raise issues of reproducibility, is mostly animal based and does not necessarily provide an understanding of the underlying mechanisms of toxicity. From an ethical and scientific viewpoint, a paradigm shift is required to deliver testing strategies that enable reliable, animal‐free hazard and risk assessments, which are based on a mechanistic understanding of chemical toxicity and make use of exposure science and epidemiological data. This shift will require a new philosophy, new data, multidisciplinary expertise and more flexible regulations. Re‐engineering of available data is also deemed necessary as data should be accessible, readable, interpretable and usable. Dedicated training to build the capacity in terms of expertise is necessary, together with practical resources allocated to education. The dialogue between risk assessors, risk managers, academia and stakeholders should be promoted further to understand scientific and societal needs. Genuine interest in taking risk assessment forward should drive the change and should be supported by flexible funding. This publication builds upon presentations made and discussions held during the break‐out session ‘Advancing risk assessment science – Human health’ at EFSA's third Scientific Conference ‘Science, Food and Society’ (Parma, Italy, 18–21 September 2018)., EFSA Journal, 17 (S1), ISSN:1831-4732, Proceedings of the Third EFSA Scientific Conference: Science, Food and Society