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Background: Haff disease is unexplained rhabdomyolysis caused by consumption of fishery products in the previous 24 h. It was first identified in Europe in 1924 but the condition is extremely rare in China. Here we describe a past outbreak of acute food borne muscle poisoning that occurred in Guangdong Province (South China) in 2009. Methods: The first full outbreak of Haff disease reported in Jiangsu Province (East China) in 2010, indicated that the incidence of the disease may be increasing in China. We, therefore first retrospectively reviewed epidemiologic, trace-back, environmental studies, and laboratory analyses, including oral toxicity testing to ascertain risk and chemical analysis to identify toxin(s), from the 2009 Guangdong outbreak. Then we compared data from the 2009 outbreak with data from all other Haff disease outbreaks that were available. Results: Clinical symptoms and laboratory findings indicated that the 2009 Guangdong outbreak disease was consistent with rhabdomyolysis. Epidemiologic, trace-back, environmental studies and laboratory analyses implied that the disease was caused by freshwater Pomfrets consumed prior to the onset of symptoms. We also identified common factors between the 2009 Guangdong outbreak and previous Haff disease outbreaks reported around the world, while as with other similar outbreaks, the exact etiological factor(s) of the disease remains unknown. Conclusions: The 2009 Guangdong outbreak of 'muscle poisoning' was retrospectively identified as an outbreak of Haff disease. This comprised the highest number of cases reported in China thus far. Food borne diseases emerging in this unusual form and the irregular pattern of outbreaks present an ongoing public health risk, highlighting the need for improved surveillance and diagnostic methodology. [ABSTRACT FROM AUTHOR]

Shantou, China, is one of the endemic regions of esophageal cancer (EC) in the coastal areas, but the relationship between the multiple exposures of total N-nitroso compounds (TNOCs) and the high risk of EC to date is unclear. This study is to estimate the potential integrative role of multiple exposures of environmental and endogenous TNOC on the EC risk. We collected randomly the samples of 72 h diet and 24 h urine from 256 healthy male (aged 30–65 years) in the high- and low-risk area for EC, and determined the contents of TNOC and 4 N-nitrosamino acids (NAAs) by a method of chemical fission-Thermal Energy Analyzer (TEA) and gas chromatography — TEA, respectively. We used TNOC and NAAs index to evaluate the integrative effect of multiple TNOC exposures on the EC risk by a logistic model. TNOC intake and urinary TNOC content were higher in the high-risk subjects than that in the low-risk subjects by 1.60 μmol/day and 1.45 μmol/L, respectively. TNOC intake, urinary TNOC content and its interaction were significant factors involved in the higher risk of EC (R 2 =0.685, p =0.000) with predicted Correct Class of 85.6%. The risk of the occurrence of a larger SMR of EC may increase by 4.841-fold for every 1 μmol/day increase in TNOC intake (95% CI 2.370–9.888, p =0.000) and by 4.113-fold for every 1 μmol/L increase in urinary TNOC content (95% CI 2.108–8.023, p =0.000), respectively. The integrally role of multiple exposures of TNOC in environment and in vivo may increase the risk of EC in the coastal areas in eastern Guangdong, China. [Copyright &y& Elsevier]