Institute for Research on Environment and Sustainability, Devonshire Building, University of Newcastle upon Tyne, Newcastle upon Tyne, NE17RU, UK.
Toxicol Appl Pharmacol. 2013 Aug 1;270(3):209-17. doi: 10.1016/j.taap.2010.11.008. Epub 2010 Nov 21.
Nitrite is widely consumed from the diet by animals and humans. However the largest contribution to exposure results from the in vivo conversion of exogenously derived nitrate to nitrite. Because of its potential to cause to methaemoglobin (MetHb) formation at excessive levels of intake, nitrite is regulated in feed and water as an undesirable substance. Forages and contaminated water have been shown to contain high levels of nitrate and represent the largest contributor to nitrite exposure for food-producing animals. Interspecies differences in sensitivity to nitrite intoxication principally result from physiological and anatomical differences in nitrite handling. In the case of livestock both pigs and cattle are relatively susceptible. With pigs this is due to a combination of low levels of bacterial nitrite reductase and hence potential to reduce nitrite to ammonia as well as reduced capacity to detoxify MetHb back to haemoglobin (Hb) due to intrinsically low levels of MetHb reductase. In cattle the sensitivity is due to the potential for high dietary intake and high levels of rumen conversion of nitrate to nitrite, and an adaptable gut flora which at normal loadings shunts nitrite to ammonia for biosynthesis. However when this escape mechanism gets overloaded, nitrite builds up and can enter the blood stream resulting in methemoglobinemia. Looking at livestock case histories reported in the literature no-observed-effect levels of 3.3mg/kg body weight (b.w.) per day for nitrite in pigs and cattle were estimated and related to the total daily nitrite intake that would result from complete feed at the EU maximum permissible level. This resulted in margins of safety of 9-fold and 5-fold for pigs and cattle, respectively. Recognising that the bulkiness of animal feed limits their consumption, these margins in conjunction with good agricultural practise were considered satisfactory for the protection of livestock health. A human health risk assessment was also carried out taking into account all direct and indirect sources of nitrite from the human diet, including carry-over of nitrite in animal-based products such as milk, eggs and meat products. Human exposure was then compared with the acceptable daily intake (ADI) for nitrite of 0-0.07 mg/kg b.w. per day. Overall, the low levels of nitrite in fresh animal products represented only 2.9% of the total daily dietary exposure and thus were not considered to raise concerns for human health. It is concluded that the potential health risk to animals from the consumption of feed or to man from eating fresh animal products containing nitrite, is very low.
亚硝酸盐广泛存在于动物和人类的饮食中。然而，暴露的最大来源是外源性硝酸盐在体内转化为亚硝酸盐。由于摄入过量可能导致高铁血红蛋白（MetHb）形成，亚硝酸盐在饲料和水中被作为一种不良物质进行监管。饲料和受污染的水已被证明含有高水平的硝酸盐，是食源性动物接触亚硝酸盐的最大来源。不同物种对亚硝酸盐中毒的敏感性差异主要源于其对亚硝酸盐处理的生理和解剖学差异。对于家畜，猪和牛都相对易感。对于猪，这是由于其细菌亚硝酸盐还原酶水平低，因此有将亚硝酸盐还原为氨的潜力，以及由于内在的低 MetHb 还原酶水平而降低了将 MetHb 解毒回血红蛋白（Hb）的能力。对于牛，其敏感性是由于高膳食摄入和瘤胃中硝酸盐向亚硝酸盐的高转化率，以及适应性强的肠道菌群在正常负荷下将亚硝酸盐分流用于生物合成。然而，当这种逃逸机制超载时，亚硝酸盐就会积累并进入血液，导致高铁血红蛋白血症。从文献中报告的家畜病例历史来看，估计了猪和牛每天每公斤体重 3.3 毫克（b.w.）的亚硝酸盐无观察到效应水平，并将其与欧盟最大允许水平下完全饲料的总日亚硝酸盐摄入量相关联。这导致猪和牛的安全系数分别为 9 倍和 5 倍。认识到动物饲料的体积限制了其摄入量，这些安全系数结合良好的农业实践，被认为足以保护家畜健康。还进行了人类健康风险评估，考虑了人类饮食中亚硝酸盐的所有直接和间接来源，包括动物源性产品（如牛奶、鸡蛋和肉类产品）中亚硝酸盐的残留。然后将人类暴露与亚硝酸盐的每日允许摄入量（ADI）0-0.07 毫克/公斤体重/天进行比较。总的来说，新鲜动物产品中的亚硝酸盐含量很低，仅占总日膳食暴露量的 2.9%，因此不会对人类健康构成担忧。结论是，动物通过摄入饲料或人类通过食用含有亚硝酸盐的新鲜动物产品而接触亚硝酸盐，对动物健康的潜在风险非常低。
