Food fraud and the perceived integrity of European food imports into China.

BACKGROUND/AIMS: Persistent incidents of food fraud in China have resulted in low levels of consumer trust in the authenticity and safety of food that is domestically produced. We examined the relationship between the concerns of Chinese consumers regarding food fraud, and the role that demonstrating authenticity may play in relieving those concerns. METHODS: A two-stage mixed method design research design was adopted. First, qualitative research (focus groups n = 7) was conducted in three Chinese cities, Beijing, Guangzhou and Chengdu to explore concerns held by Chinese consumers in relation to food fraud. A subsequent quantitative survey (n = 850) tested hypotheses derived from the qualitative research and theoretical literature regarding the relationship between attitudinal measures (including risk perceptions, social trust, and perceptions of benefit associated with demonstrating authenticity), and behavioral intention to purchase "authentic" European products using structural equation modelling. RESULTS: Chinese consumers perceive food fraud to be a hazard that represents a food safety risk. Food hazard concern was identified to be geographically influenced. Consumers in Chengdu (tier 2 city) possessed higher levels of hazard concern compared to consumers in Beijing and Guangzhou (tier 1). Structural trust (i.e. trust in actors and the governance of the food supply chain) was not a significant predictor of attitude and intention to purchase authenticated food products. Consumers were shown to have developed 'risk-relieving' strategies to compensate for the lack of trust in Chinese food and the dissonance experienced as a consequence of food fraud. Indexical and iconic authenticity cues provided by food manufacturers and regulators were important elements of product evaluations, although geographical differences in their perceived importance were observed. CONCLUSIONS: Targeted communication of authenticity assurance measures, including; regulations; enforcement; product testing; and actions taken by industry may improve Chinese consumer trust in the domestic food supply chain and reduce consumer concerns regarding the food safety risks associated with food fraud. To support product differentiation and retain prestige, European food manufactures operating within the Chinese market should recognise regional disparities in consumer risk perceptions regarding food fraud and the importance of personal risk mitigation strategies adopted by Chinese consumers to support the identification of authentic products.

Critical review of methods for risk ranking of food-related hazards, based on risks for human health.

This study aimed to critically review methods for ranking risks related to food safety and dietary hazards on the basis of their anticipated human health impacts. A literature review was performed to identify and characterize methods for risk ranking from the fields of food, environmental science and socio-economic sciences. The review used a predefined search protocol, and covered the bibliographic databases Scopus, CAB Abstracts, Web of Sciences, and PubMed over the period 1993-2013. All references deemed relevant, on the basis of predefined evaluation criteria, were included in the review, and the risk ranking method characterized. The methods were then clustered-based on their characteristics-into eleven method categories. These categories included: risk assessment, comparative risk assessment, risk ratio method, scoring method, cost of illness, health adjusted life years (HALY), multi-criteria decision analysis, risk matrix, flow charts/decision trees, stated preference techniques and expert synthesis. Method categories were described by their characteristics, weaknesses and strengths, data resources, and fields of applications. It was concluded there is no single best method for risk ranking. The method to be used should be selected on the basis of risk manager/assessor requirements, data availability, and the characteristics of the method. Recommendations for future use and application are provided.

STILL FEBRILE - A RARE CAUSE OF JOINT PAIN.

A 35-year-old woman presented to our emergency department complaining of arthralgia, rash, fevers, and muscle weakness for the past year. These symptoms initially began as unilateral upper lip swelling, which then progressed to a facial rash and orbital swelling over two weeks with associated fevers, which eventually subsided. The patient then began having fluctuating arthralgia and muscle weakness with associated rash and subjective fevers. She had rheumatologic evaluation several months prior to our encounter at another facility, which failed to reveal an explanation for her symptoms. During this workup, antinuclear antibodies (ANA), rheumatoid factor (RF), and complement levels were normal with elevated erythrocyte sedimentary rate (ESR) and C-reactive protein (CRP). On arrival to our hospital, she complained of symmetric polyarthritis involving the ankles, knees, shoulders, and hands, and proximal upper and lower extremity weakness with difficulty rising from a seated position. On examination she was noted to have an evanescent rash on bilateral extremities and her abdomen. Cardiac exam revealed no murmurs. Laboratory testing was significant for anemia, hyperferritinemia, leukocytosis, with negative RF and ANA. Transaminitis was not present. The patient's fevers resolved and her symptoms improved during hospitalization. She was started on prednisone 60mg daily and discharged with follow up in the rheumatology clinic to initiate therapy with the IL-1 antagonist anakinra.

Phylogenetic analysis of spring virema of carp virus reveals distinct subgroups with common origins for recent isolates in North America and the UK.

Genetic relationships between 35 spring viremia of carp virus (SVCV) genogroup Ia isolates were determined based on the nucleotide sequences of the phosphoprotein (P) gene and glycoprotein (G) genes. Phylogenetic analysis based on P gene sequences revealed 2 distinct subgroups within SVCV genogroup Ia, designated SVCV Iai and Iaii, and suggests at least 2 independent introductions of the virus into the USA in 2002. Combined P- and G-sequence data support the emergence of SVCV in Illinois, USA, and in Lake Ontario, Canada, from the initial outbreak in Wisconsin, USA, and demonstrate a close genetic link to viruses isolated during routine import checks on fish brought into the UK from Asia. The data also showed a genetic link between SVCV isolations made in Missouri and Washington, USA, in 2004 and the earlier isolation made in North Carolina, USA, in 2002. However, based on the close relationship to a 2004 UK isolate, the data suggest than the Washington isolate represents a third introduction into the US from a common source, rather than a reemergence from the 2002 isolate. There was strong phylogenetic support for an Asian origin for 9 of 16 UK viruses isolated either from imported fish, or shown to have been in direct contact with fish imported from Asia. In one case, there was 100% nucleotide identity in the G-gene with a virus isolated in China.

A phagocytic challenge with IgG-coated erythrocytes depresses macrophage respiratory burst and phagocytic function by different mechanisms.

A phagocytic challenge with IgG-coated erythrocytes (EIgG) previously has been shown to cause impaired macrophage respiratory burst capacity and FcgammaR-mediated phagocytic function. Because both the respiratory burst and FcgammaR-mediated phagocytosis are dependent on the release of arachidonate (AA), we evaluated the effects of impaired AA release on the depression of macrophage function caused by a phagocytic challenge. Challenge with EIgG caused a depression of A23187-stimulated AA release that was associated with impaired phorbol myristate acetate (PMA)-stimulated H2O2 production and FcgammaR-mediated phagocytic function. In contrast, challenge with IgG-coated glass beads (BIgG) had no effect on either AA release or H2O2 production but did depress phagocytic function. Exogenous AA prevented the depression of H2O2 production but had no effect on phagocytic function. Phospholipase A2 (PLA2) activity was depressed under conditions where AA release was impaired. The depression of phagocytic function was correlated with a depression of both EIgG binding and FcgammaR expression. Thus, a phagocytic challenge with EIgG results in macrophage dysfunction by depressing PLA2 activity and depleting FcgammaR.

Role of an oxidative stress in the macrophage dysfunction caused by erythrophagocytosis.

A phagocytic challenge with immunoglobulin G (IgG)-coated erythrocytes (EIgGs) has been shown to cause a subsequent depression of macrophage respiratory burst capacity and phagocytic function. The present study evaluated the hypothesis that this macrophage dysfunction is caused by an oxidative stress. An oxidative stress induced by ferric ammonium citrate (FAC) plus cumene hydroperoxide (CHP) caused a depression of macrophage function that was attenuated by antioxidants and iron chelators. In contrast, the same antioxidants and iron chelators did not alter changes caused by a challenge with EIgGs. EIgG challenge caused an increase in lipid peroxidation but failed to deplete glutathione (GSH) or decrease the activity of glyceraldehyde-3-phosphate dehydrogenase (GA-3-PD), suggesting that there was only a slight oxidative stress. Inhibition of the Fc gamma receptor (Fc gammaR) stimulated respiratory burst by removing calcium during the challenge did not attenuate the changes caused by an EIgG challenge. A phagocytic challenge with nonerythrocyte particles, IgG-coated beads (BIgGs), did not depress the respiratory burst capacity but did depress phagocytic function. Fc gammaR expression was depressed following a phagocytic challenge but not an oxidative stress. Thus, an oxidative stress can depress macrophage function, but the dysfunction caused by a phagocytic challenge with EIgGs involves Fc gammaR depletion and the erythrocyte contents rather than an oxidative stress.

Lysosomotropic agents ameliorate macrophage dysfunction following the phagocytosis of IgG-coated erythrocytes: a role for lipid peroxidation.

Phagocytosis of IgG-coated erythrocytes (EIgG) can depress several macrophage functions. Our previous studies have suggested that this macrophage dysfunction may be due to an oxidative stress caused by the interaction of hemoglobin-derived iron with superoxide and/or hydrogen peroxide. Since lysosomotropic agents are capable of altering iron handling by macrophages, the present study evaluated the ability of these agents to prevent the macrophage dysfunction and lipid peroxidation caused by a phagocytic challenge with EIgG. Elicited rat peritoneal macrophages showed a depression of PMA-stimulated hydrogen peroxide production, calcium ionophore-stimulated arachidonate release and Fc receptor-mediated phagocytosis. The lysosomotropic agents; chloroquine, quinacrine, ammonium chloride and methylamine all prevented the depression of hydrogen peroxide production and arachidonate release but did not alter the depression of phagocytic function. These agents also prevented the increase in lipid peroxidation products caused by a phagocytic challenge with EIgG. These results suggest that the ability of lysosomotropic agents to prevent some aspects of macrophage dysfunction after a phagocytic challenge may be due to their ability to block the oxidative stress caused by the challenge.

Macrophage dysfunction following the phagocytosis of IgG-coated erythrocytes: production of lipid peroxidation products.

The phagocytosis of erythrocytes may contribute to the increased susceptibility to life-threatening infections in patients with burn injury, sickle cell anemia, and malaria. The phagocytosis of immunoglobulin G-coated erythrocytes (EIgG) is followed by a transient depression of several macrophage functions including phagocytosis, respiratory burst capacity, and killing of bacteria. The present study suggests the possibility that after erythrophagocytosis hemoglobin-derived iron conspires with reactive oxygen products of the macrophage respiratory burst to cause oxidant damage to the phagocyte. Challenge of elicited peritoneal macrophages with EIgG phagocytosis was followed by an increase in lipid peroxidation as assessed by thiobarbituric acid-reactive substances (TBARS). Doses of EIgG associated with increased TBARS also caused a depression of Fc receptor-mediated phagocytosis and phorbol myristate acetate (PMA)-stimulated hydrogen peroxide production. Time course experiments demonstrated that the increase in TBARS coincided with the depression of macrophage function. There was no increase in TBARS following the phagocytosis of IgG-coated erythrocyte ghosts, suggesting that hemoglobin iron is involved in the generation of TBARS. The phagocytosis of erythrocyte ghosts did not depress macrophage function. Since complement receptor-mediated phagocytosis does not stimulate the respiratory burst, the role of the respiratory burst in causing lipid peroxidation was assessed using the phagocytosis of complement-coated erythrocytes. Phagocytic challenge with complement-coated erythrocytes caused neither an increase in TBARS nor a depression of macrophage function. However, there was an increase in TBARS when the respiratory burst was stimulated with PMA following complement receptor-mediated phagocytosis of erythrocytes. These results suggest that hemoglobin iron and phagocyte-generated oxidants collaborate to cause the depression of macrophage function following EIgG phagocytosis.