[Analysis of heavy metals monitoring results in food in Shaoxing in 2014].

OBJECTIVE: To investigate heavy metals contamination level in food in Shaoxing, and to provide basis evidence for supervising heavy metals pollution in food and environmental pollution control in Shaoxing. METHODS: Food samples in 2014 were detected for lead, cadmium, mercury, arsenic, nickel, copper and chromium by national standard methods, and the results were evaluated by GB 2762-2012 Pollutants limits in food. RESULTS: 1384 samples from 10 food categories were collected and tested for lead, cadmium, mercury and arsenic, the over standard rates were 2.0%, 3.0%, 1.5% and 0.22%, respectively, the median were 0.019, 0.0085, 0.0024 and 0.015 mg/kg, respectively; 273 samples were collected and tested for nickel, the detection rate was 48.4%, the median was 0.010 mg/kg; 255 samples were collected and tested for chromium, the detection rate was 14.9%, the median was 0.0050 mg/kg; 486 samples were collected and tested for copper, the detection rate was 94.0%, the median was 1.34 mg/kg. The heavy metals over standard rate of aquatic products, animal internal organs and grain were relatively high, 16.9%, 7.9% and 7.3% cadmium in swimming crabs exceeded standard seriously, the over standard rate was 38.9%. CONCLUSION: The overall pollution of heavy metals in food are not high in Shaoxing in 2014, but some food (aquatic products, animal internal organs and grain) pollution are relatively outstanding, and have the over standard problems of lead, cadmium, mercury and arsenic.

[The characteristics and trends of acute pesticide poisoning of Shaoxing in 2006 to 2011].

OBJECTIVE: To describe the epidemiological characteristics of acute pesticide poisoning in Shaoxing, China during 2006-2011 and to provide a reference for the prevention and control of pesticide poisoning. METHODS: The data on pesticide poisoning in Shaoxing during 2006-2011 were obtained from the China Information System for Disease Control and Prevention and were then analyzed. RESULTS: A total of 2024 cases of acute pesticide poisoning were reported in Shaoxing during 2006-2011, and 44 cases were missed, accounting for 2.1% (44/2068) of all cases. Among the 2024 cases, 119 (5.9%) died; the fatality rates of productive poisoning and unproductive poisoning were 1.0% (3/289) and 6.7% (116/1735), respectively. The reported cases included 1038 (51.3%) females and 986 (48.7%) males, and there were no significant differences in the ratio between male and female cases of acute pesticide poisoning from 2006 to 2011 (χ2 = 9.16, P = 0.10). The 2024 cases had a mean age of 47.0±18.7 years; the male cases had a significantly higher mean age than the female cases (50.7±19.0 vs 43.4±17.8 years, t = 9.01, P < 0.001). Among the 2024 cases, 289 (14.3%) suffered productive poisoning, and 1735 (85.7%) suffered unproductive poisoning. In the 986 male cases, 219 (22.2%) suffered productive poisoning; in the 1038 female cases, 968 (93.3%) suffered unproductive poisoning. The pesticides that caused poisoning included insecticide (86.7%, 1754/2024), herbicide (5.1%, 104/2024), rodenticide (3.6%, 72/2024), and bactericide, mixed preparation, biochemical pesticides, and other four categories of pesticides (4.6%, 94/2024); of the 1754 cases caused by insecticide, 1455 (83.0%) were attributed to organophosphorus insecticide. CONCLUSION: The incidence of unproductive acute pesticide poisoning is high in Shaoxing, and it mainly affects females. Most cases of acute pesticide poisoning are aged 30∼60 years. Insecticide is the main cause of poisoning. It is necessary to enhance health knowledge popularization and safety management of pesticides.

Lead induces oxidative stress, DNA damage and alteration of p53, Bax and Bcl-2 expressions in mice.

Oxidative stress is considered as a possible molecular mechanism involved in lead toxicity. This study was carried out to investigate whether lead acetate could induce oxidative stress in mice, and the following damages as well. Lead acetate was given orally to mice for 4 weeks at doses of 0, 10, 50, 100mg/kg body weight every other day, respectively. Production of reactive oxygen species (ROS) and malondialdehyde (MDA) were measured as indicators of oxidative stress. DNA damage in peripheral blood lymphocytes was determined by comet assay. Ultrastructure alteration was detected using transmission electron microscopy. The alterations of p53, Bax, and Bcl-2 expression were determined by western blotting. The results showed that lead acetate significantly increased the levels of ROS and MDA in mice. Meanwhile, severe DNA damage and ultrastructure alterations were obviously observed. In addition, p53 and Bax expressions increased and the imbalance of Bax/Bcl-2 occurred. Therefore, it strongly suggests that lead may induce oxidative stress and change the expressions of apoptosis-related proteins in mouse liver.

Tributyltin induces DNA damage as well as oxidative damage in rats.

In this study, oxidative and DNA damage were measured synchronously after Sprague-Dawley rats were exposed to different dosages of tributyltin (TBT) for 3 and 7 consecutive days. Oxidative damage was measured by analyzing the production of hepatic reactive oxygen species (ROS), the activity of superoxide dismutase (SOD), and the content of malondialdehyde (MDA). DNA damage was measured by single-cell gel electrophoresis (comet assay). After 3 days of exposure, significant differences in ROS production could only be seen between the control and the highest dosage group (10 mg/kg BW d), although after 7 days of treatment, ROS production increased in a dose-dependent manner. SOD activity increased with dosage after 3 days of exposure and decreased with dosage after 7 days of exposure. TBT also induced significant production of MDA after 7 days of exposure. The changes in ROS, SOD, and MDA found in this study suggest that the antioxidative systems of rats were activated by TBT in the first 3 days of exposure but had become exhausted by 7 days of exposure. In the comet assay, the number of cells with damaged DNA in rats treated with TBT increased with dosage of TBT. The most likely mechanism of the DNA breakage induced by TBT is oxidative damage. It can be concluded that exposure of TBT can promote both oxidative and DNA damage in mammals in vivo.