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Food Additives & Contaminants: Part B: Surveillance Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/tfab20
Lead and cadmium levels in cattle muscle and edible tissues collected from a slaughter slab in Nigeria a
a
b
V.O. Adetunji , I.O. Famakin & J. Chen a
Department of Veterinary Public Health and Preventive Medicine, University of Ibadan, Ibadan, Nigeria b
Department of Food Science & Technology, The University of Georgia, Griffin, GA, USA Accepted author version posted online: 10 Oct 2013.Published online: 28 Nov 2013.
Click for updates To cite this article: V.O. Adetunji, I.O. Famakin & J. Chen (2014) Lead and cadmium levels in cattle muscle and edible tissues collected from a slaughter slab in Nigeria, Food Additives & Contaminants: Part B: Surveillance, 7:2, 79-83, DOI: 10.1080/19393210.2013.848942 To link to this article: http://dx.doi.org/10.1080/19393210.2013.848942
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Food Additives & Contaminants: Part B, 2014 Vol. 7, No. 2, 79–83, http://dx.doi.org/10.1080/19393210.2013.848942
Lead and cadmium levels in cattle muscle and edible tissues collected from a slaughter slab in Nigeria V.O. Adetunjia*, I.O. Famakina and J. Chenb a
Department of Veterinary Public Health and Preventive Medicine, University of Ibadan, Ibadan, Nigeria; bDepartment of Food Science & Technology, The University of Georgia, Griffin, GA, USA
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(Received 9 July 2013; accepted 22 September 2013) Contamination levels of lead (Pb) and cadmium (Cd) in muscles, liver and kidney of 50 randomly selected, freshly slaughtered cattle in Ogun State, Nigeria were assessed using an official procedure and atomic absorption spectrophotometry. Results showed that Pb and Cd were present in all of the tested samples. Mean Pb concentrations were 0.721 ± 0.180 mg kg−1, 0.809 ± 0.220 mg kg−1 and 0.908 ± 0.422 mg kg−1 in muscle, liver and kidney tissues, respectively. Mean Cd concentrations were 0.157 ± 0.049 mg kg−1, 0.172 ± 0.071 mg kg−1 and 0.197 ± 0.070 mg kg−1 in muscle, liver and kidney tissues, respectively. Pb and Cd levels in muscle versus kidney tissues and also in liver versus kidney samples were significantly different (p < 0.05). Mean Pb concentrations in all tested tissues were significantly higher than the International Standards while the mean Cd concentrations in liver and kidney samples were within the limits of these standards. Keywords: lead; cadmium; heavy metal; cattle muscle; edible tissues; cattle carcasses
Introduction Heavy metal pollution is a growing environmental problem on a global scale (Matthew et al. 2002) and the risk associated with exposure to heavy metal presence in food products had aroused widespread concerns for human health. The increase in heavy metal pollution in the ecosystem is caused by various human and natural activities (Srikanth et al. 2004), including dumping of wastes, process spillages, use of agricultural pesticides, movement of contaminants into a fertile land and dispersal of sewage mire. Symptoms from exposures to heavy metals such as lead (Pb) and cadmium (Cd) are nonspecific and may be subtle, and someone with elevated blood Pb levels may have no symptoms (Mycyk et al. 2005). Observable symptoms include hyperactivity or stunted growth in infants and teens. Accumulation of Pb in the human body can also cause reproductive problems, high blood pressure, nervous disorders, oligospermia in males, abortion in females and amnesia in adults. In severe cases, it can lead to seizures, coma and even death (Wagner 1995; Kocak et al. 2005). Implementation of new technologies in food production and processing technology has increased the chances of contamination of food with various environmental pollutants, especially heavy metals. Ingestion of these contaminants by animals causes deposition in meat. Due to the grazing of animals on contaminated soil, higher levels of metals have been found in beef and mutton (Sabir et al. *Corresponding author. Email:
[email protected] © 2013 Taylor & Francis
2003) as a result of bioaccumulation. A previous study in Spain has recorded higher than the maximum levels of toxic metals including Pb and Cd in meat products (Gonzalez-Waller et al. 2006). Cattle muscle and tissues form a significant part of human diet for the supply of proteins. Offals, such as liver, kidney and spleen, are edibles in developing countries like Nigeria and often accumulate higher concentration of toxic metals than most foods. On the other hand, the contents of toxic metals in muscles are mostly low (Alnaemi 2011). Studies of toxic metals in tissues and muscles have been carried out in many countries, e.g. Finland (Tahvonen & Kumpulainen 1994), Canada (Salisbury et al. 1991) and Iraq (Al-naemi 2011). However, the report on the levels of heavy metal contamination in muscle and edible tissues from Nigeria is scarce. This study determined the levels of Pb and Cd in cattle muscles, liver and kidney tissues and compared the findings with those found in other geological locations and maximum limits. Materials and methods Sampling Samples of this study were collected from Oluwanisola Cattle market which is located at Kraal Bus Stop, Ogun State along the Lagos–Ibadan Expressway in Nigeria. The market has an abattoir on site that slaughters an average of 300 cattle daily. Fifty cattle were selected randomly on the slaughter slab during a 5 week period in the months of
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June and July 2012. Samples of liver, kidney and muscle tissue were harvested in duplicates from the selected animals. At least 20 g of each sample was collected and placed into polythene bags (Whirl-Pak®, SKS science products, OH, USA). Samples were transported on the same day to the laboratory and stored at –20°C until analysis within 48 h.
Table 1. Operational parameters for Pb and Cd measurement in tissue samples. Parameter Wavelength Slit width Sample volume Limits of detection Recovery range
Pb
Cd
228.8 nm 0.7 nm 20 ml 0.025 mg kg−1 90.6–100.0%
283.3 nm 0.7 nm 20 ml 0.0025 mg kg−1 82.0–100.0%
Sample preparation
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The collected samples were allowed to thaw at room temperature (26–28°C) after which fat tissue of the samples was removed and 10 g was dried in an oven at 70°C for 3 days (Tyler Griffin Company, Pennsylvania, USA). After drying, individual samples were crushed to powder using a mortar and pestle. Wet digestion Wet digestion of the samples was done using a method previously described by Richards (1968). Exactly 0.5 g of each milled sample was placed into a 100 ml digestion flask (Global spec, NY, USA) and 10 ml concentrated nitric acid (Sigma-Aldrich, Steinheim, Germany) was added. The contents of the digestion flasks were preheated on a hot plate (Thermo Scientific, New Hampshire, USA), for 20 min and then cooled to 28°C at room temperature. A total volume of 5 ml of perchloric acid was subsequently added into the solution and the mixture was heated at 400°C until white fumes appeared and the sample volume reduced to 3 ml. The final volume was made up to 25 ml by adding deionised water and then transferred to lidded glass test tubes for analysis.
manufacturer (Table 1). Quality control was ascertained by analysis of reagent and procedural blanks. Multiple readings were taken per sample to establish accuracy and acceptable correlation coefficients of at least 0.9997 were obtained for all analysis. The limit of detection was calculated as three times the SD of the mean reagent blanks. The limit of quantification was determined as 10 times the SD of reagent blanks. Statistical analysis One-way analysis of variance (ANOVA) was used to establish significant differences between mean levels of Pb and Cd present in the muscle, liver and kidney at 95% confidence limits. Student’s t-test was used in testing significant differences in their means using IBM SPSS 20.0 (SPSS Inco. Chicago, IL, USA). One Sample Student’s t-test was used to compare the levels of Pb and Cd present in tissues with the International standards (Commission of the European Communities [EC] 2006; Codex Alimentarius Commission 2007). Results and discussion Pb levels in muscle, liver and kidney samples
Reagents, standards and apparatus All glassware used was washed with Ariel detergent (Unilever, Lagos, Nigeria), thoroughly rinsed with deionised water and sterilised at 120°C for 15 min before use. All chemicals and reagents were of analytical standard/ grade. Deionised water was used for all analysis. Pb and Cd standards were prepared by diluting the commercial products (100 mg l–1) in 0.1N HNO3. A Perkin Elmer Analyst 200 Atomic Absorption Spectrophotometer equipped with a graphite furnace and lamp was used for the determination of Pb and Cd levels (Perkin Elmer, Massachusetts, USA). Calibration curves for Pb and Cd were determined using a blank and samples with an increasing amount of working standards of the heavy metals. Mean recoveries for Pb and Cd were 90.6–100.0% and 82–100.0%, respectively, with a relative standard deviation (SD) of 2.3–5.4% and 1.3–5.1%, respectively. The operating parameters for Pb and Cd quantification were set as recommended by the
The levels of Pb in muscle ranged between 0.265 and 1.044 mg kg−1, with a mean concentration of 0.721 mg kg−1. The levels in liver ranged between 0.415 and 1.480 mg kg−1 with an average of 0.809 mg kg−1, while the levels in kidney ranged between 0.417 and 3.180 mg kg−1 with a mean concentration of 0.908 mg kg−1 (Table 2). This study also revealed that Pb was detected in all analysed tissues and a significant difference (p < 0.05) in the concentration of Pb in muscle versus kidney and also in liver versus kidney was observed. Generally, kidneys contained higher Pb concentrations than livers. Similar observations had been made with bovine kidney, liver and muscle samples in Jamaica (Nriagu et al. 2009) and the mean concentrations of Pb were found to be highest in the kidney, followed by liver and muscle. Similar to the findings of the present study, sheep and horses have shown to accumulate Pb in their kidneys and livers (Liu 2003). An earlier study by AbouDonia (2008) detected 0.490 mg kg−1 of Pb in kidney and
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Table 2. Comparison of mean Pb concentrations in muscle, liver and kidney samples with international standards (mg kg−1). Carcass part Muscle (n = 50) Liver (n = 50) Kidney (n = 50)
Measured
ML (Codex Alimentarius Commission)
ML (EC)
No. of samples exceeding ML
0.721 ± 0.180bc 0.809 ± 0.220b 0.908 ± 0.422a
0.1–0.5 0.1–0.5 0.1–0.5
0.1 0.5 0.5
50 (100%) 47 (94%) 44 (88%)
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Notes: ML: Maximum limit. Mean lead levels are expressed as mean ± SD. Means with the same letters are not statistically significant at p < 0.05.
0.109 and 0.364 mg kg−1 in liver from cattle beside heavy traffic areas and urban areas, respectively. Pb levels in muscle, liver and kidney tissues sampled in the present study are significantly higher than the maximum limits set by the Codex Alimentarius Commission (2007) and by the EC (2006). Aranha et al. (1994) also reported higher than limit concentrations of Pb in liver and kidney of animals in Brazil. This finding is a public health concern since Pb is a neurotoxin affecting mental development and also interferes with metabolism of calcium and vitamin D. In addition, Pb has also been shown to inhibit haemoglobin formation, thereby causing anaemia. Cd levels in muscle, liver and kidney samples Cd was detected in all the carcass parts sampled in the present study and the levels in muscle tissue ranged between 0.043 and 0.279 mg kg−1, with a mean concentration of 0.156 mg kg−1. The levels of Cd in liver ranged between 0.047 and 0.399 mg kg−1 with an average of 0.172 mg kg−1 while the levels in kidney ranged between 0.090 and 0.379 mg kg−1 with a mean concentration of 0.197 mg kg−1 (Table 3). The highest Cd content was found in the liver followed by the kidney. There was a significant difference in the concentrations of Cd in the muscle versus kidney, as well as in the liver versus kidney samples (p < 0.05). The concentrations of Cd in the liver and kidney samples were lower than the maximum limits of 0.5 and 1 mg kg−1 in liver and kidney of the EC (2006), except for muscle tissue (Table 3). These findings are similar to reports of Bala et al. (2012); Akan et al. (2010) found Cd concentrations in liver, kidney and
Table 3. Comparison of mean Cd concentrations in muscle, liver and kidney samples with International Standards (mg kg−1). Carcass part Muscle tissue (n = 50) Liver (n = 50) Kidney (n = 50)
Measured
No. exceeding limits (%)
ML (EC)*
0.157 ± 0.049bc
49 (98%)
0.05
0.172 ± 0.071b 0.197 ± 0.070a
0 (0%) 0 (0%)
0.5 1.25
Notes: ML: Maximum limit. Mean cadmium levels are expressed as mean ± SD. Means with the same letters are not statistically significant at p < 0.05. *Codex ML not available.
meat of beef, mutton, caprine and chicken samples in Nigeria lower than the 0.5 mg kg–1 maximum limit as set by FAO/WHO (2000). Cd contents of muscle, liver and kidney assayed in this study were 17.4, 2.91 and 2.01 times higher, respectively, than those sampled by Alnaemi (2011) in Iraq. However, muscle tissues sampled by Nwude et al. (2010) in Nigeria had a 1.25 times higher Cd contamination than those assayed in the present study. The presence of Cd in edible samples is of public health significance. Cd has a long biological half-life of about 30 years in humans (Bellies 1994). It damages the proximal tubules of nephrons, leading first to leakage of low molecular weight proteins and essential ions like calcium into the urine, with progression over time to kidney failure (Satrug et al. 2000). Even the loss of calcium caused by the adverse effect of Cd on the kidney can lead to the weakening of the bones resulting in itai-itai disease (Staessen et al. 1999). Cattle and other animals serve as bio-indicators of environmental contamination of heavy metals (Miranda et al. 2009). The results of this study might reflect undue levels of heavy metal exposure in a local environment. The animals could potentially have picked heavy metals from the environment, given the challenges of free-range grazing, scavenging in open waste dumps for fodder, drinking water from polluted drains and streams and exposure to atmospheric depositions, especially from automobile fumes and open burning of solid waste. Earlier, close correlation has been reported between heavy metal concentration in cattle tissues with that in soil, feed and drinking water (Sedki et al. 2003; Qiu et al. 2008). It is an established fact that non-essential elements can be transferred through food chains through environmental contamination (Rogival et al. 2007). It is therefore possible that eating habits of cattle under study lead to bioaccumulation of heavy metals in liver and kidney. Generally, toxic heavy metals such as Pb and Cd have slow rates of elimination, such that harmful levels could accumulate in tissues after prolonged exposure to even low quantities in the environment (Doyle & Spaulding 1978; Sharma et al. 1982; Humphreys 1991). Consumption of animal tissue, especially liver, has increased over the years in many parts of the world (Siddiqui et al. 2006) because of its high iron content. This consequently may result in indirect ingestion of Pb from liver, kidney and other animal tissue, thereby posing
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a serious threat to public health. Earlier reports have shown that consumption of meat of these animals may pose a serious health problem as a result of bioaccumulation of Pb in body tissues, which varies with individual and duration of Pb exposure (Kosnett 2005; Kosnett et al. 2007). Conclusions The results of this study showed that bovine kidney samples contained higher concentrations of Cd and Pb than liver samples. Also, high Pb levels were detected in some carcass parts. This has serious public health implications in view of the large population which depend on these animals as a source of proteins. However, Cd levels determined in liver and kidney were within limits. It is therefore recommended to monitor slaughtered animals in abattoirs with regard to heavy metals, to prevent consumers being exposed to heavy metal exposure from the environment. Acknowledgement The authors wish to thank the college of Agriculture, University of Ibadan, Nigeria, for providing facilities to analyse samples with atomic absorption spectrophotometric equipment.
References Abou-Donia MA. 2008. Lead concentrations in different animal muscles and consumable organs at specific localities in Cairo. Global Veterina. 2:280–284. Akan JC, Abdulrahman FI, Sodipo OA, Chiroma YA. 2010. Distribution of heavy metals in the liver, kidney and meat of beef, mutton, caprine and chicken from kasuwa shanu market in Maiduguri. Res J Appl Sci Eng Technol. 8:743–748. Al-naemi H. 2011. Estimation of lead and cadmium levels in muscles, liver and kidney of slaughtered cattle in Mosul City. Mesopotamia J Agric. 39:8–16. Aranha S, Nishkawa AM, Taka T, Salioni EMC. 1994. Cadmium and lead levels in cattle’s liver and kidney. Rev Inst Adolfo Lutz. 54:16–20. Bala A, Saulawa MA, Junaidu AU, Salihu MD, Onifade KI, Magaji AA, Anzaku SA, Faleke OO, Musawa AI, Mohammed M, et al. 2012. Detection of cadmium (Cd) residue in kidney and liver of slaughtered cattle in Sokoto Central Abattoir, Sokoto State, Nigeria. J Vet Adv. 2:168–172. Bellies RP. 1994. The metal. In: Clayton GD, Clayton FE, editors. Patty’s industrial hygiene and toxicology, Vol. 2, Part C. 4th ed. New York (NY): John Wiley and Sons; p. 256. Codex Alimentarius Commission. 2007. Joint FAO/WHO food standards programme. Codex Committee on methods of analysis and sampling, twenty-eighth session; March 5–9; Budapest. Doyle JJ, Spaulding JE. 1978. Toxic and essential trace elements in meat – a review. J Anim Sci. 47:398–419. [EC] Commission of the European Communities 2006. Commission Regulation (EC) No. 1881. Setting maximum levels for certain contaminants in foodstuffs. Off J Eur Comm. L364:5.
FAO/WHO. 2000. Report of the 32nd session of the codex committee of the food additives contaminants; March 20–24; Beijing. Gonzalez-Waller DL, Karlsson A, Caballero F, Hernandez A, Gutierrez T, Gonzalez-Igalesias M, Marino AH. 2006. Lead and cadmium in meat and meat products consumed by the population in Tenerife Islands, Spain. Food Addit Contamin. 23:757–763. Humphreys DJ. 1991. Effects of exposure to excessive quantities of lead on animals. Br Vet J. 147:18–30. Kocak S, Tokusoglu O, Aycan S. 2005. Some heavy metals and trace essential detection in canned vegetable foodstuff by differential pulse polarography. Elect J Environ Agric Field Chem. 4:871–878. Kosnett MJ. 2005. Lead. In: Brent J, Wallace K, Burkhart KB, editors. Critical care toxicology: the diagnosis and management of the acutely poisoned patient. Philadelphia (PA): Elsevier; p. 821–836. Kosnett MJ, Wedeen RP, Rothenberg SJ, Hipkins KL, Materna BL, Schwartz BS, Hu H, Woolf A. 2007. Recommendations for medical management of adult lead exposure. Environ Health Perspect. 115:463–471. Liu ZP. 2003. Lead poisoning combined with cadmium in sheep and horses in the vicinity of non-ferrous metal smelters. Sci Total Environ. 309:117–126. Matthew MM, Henke R, Atwood A. 2002. Effectiveness of commercial heavy metal chelators with new insights for the future in chelate design. J Hazard Mater. 92:129–142. Miranda M, Benedito JL, Blanco-Penedo I, López-Lamas C, Merino A, López-Alonso M. 2009. Metal accumulation in cattle raised in a serpentine-soil area: relationship between metal concentrations in soil, forage and animal tissues. J Trace Elem Med Biol. 23:231–238. Mycyk M, Hryhorczuk D, Amitai Y. 2005. Lead. In: Erickson TB, Ahrens WR, Aks S, Ling L, editors. Pediatric toxicology: diagnosis and management of the poisoned child. New York (NY): McGraw-Hill Professional; 463 pp. Nriagu J, Boughanen M, Linder A, Howe A, Grant C, Rattray R, Vutchkov M, Lalor G. 2009. Levels of As, Cd, Pb, Cu, Se and Zn in bovine kidneys and livers in Jamaica. Ecotoxicol Environ Safety. 72:564–571. Nwude DO, Okoye PAC, Babayemi JO. 2010. Heavy metal level in animal muscle tissue. A case study of Nigeria raised cattle. Res J Appl Sci. 5:146–150. Qiu CAI, Long M, Liu J, Zhu M, Zhou Q-Z, de Deng Y, Li Y, Tain YJ. 2008. Correlation between heavy metals concentration in cattle tissues and rearing environment. Chinese J Ecol. 27:202–207. Richards LA. 1968. Diagnosis and improvement of saline and alkaline soils. Agriculture Handbook No. 60. 1st ed. New Delhi: IBH Publishing Co. Rogival D, Scheirs J, Blust R. 2007. Transfer and accumulation of metals in a soil-diet-wood mouse food chain along a metal pollution gradient. Environ Pollut. 145:516–528. Sabir SM, Khan SW, Hayat I. 2003. Effect of environmental pollution on quality of meat in district Bagh, Azad Kashmir. Pak J Nutr. 2:98–101. Salisbury CDC, Chan W, Saschenbrecker PW. 1991. Multielement concentrations in liver and kidney tissues from five species of Canadian slaughter animals. J Assoc Off Anal Chem. 74:87–591. Satrug S, Haswell-Elkins MR, Moore MR. 2000. Safe levels of cadmium intake to prevent renal toxicity in human subjects. Br J Nutr. 84:791–802.
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Downloaded by [University of Arizona] at 03:27 18 December 2014
Sedki A, Lekouc N, Gamon S, Pinea A. 2003. Toxic and essential trace metals in muscle, liver and kidney of bovines from a polluted area of Morocco. Sci Total Environ. 317:201–205. Sharma RP, Street JC, Shupe JL, Bourcier DR. 1982. Accumulation and depletion of cadmium and lead in tissues and milk of lactating cows fed small amounts of these metals. J Dairy Sci. 65:972–979. Siddiqui MKJ, Jyoti S, Singh PK, Mehrotra KS, Sarangi R. 2006. Comparison of some trace elements concentration in blood, tumor free breast and tumor tissues of women with benign and malignant breast lesions: An Indian study. Environ Inter. 32:630–637. Srikanth R, Rao AM, Kumar CHS, Khanum A. 2004. Lead, cadmium, nickel, and zinc contamination of ground water
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around Hussain Sagar Lake, Hyderabad, India. Bull Environ Contam Toxicol. 50:138–143. Staessen JA, Roels HA, Emelianov D, Kuntsova T, Thyis L, Vangronsveld J. 1999. Environmental exposure to cadmium, forearm bone density, and risk of fractures: prospective population study. Public Health and Environmental Exposure to Cadmium (PheeCad) Study Group. Lancet. 353:1140–1144. Tahvonen R, Kumpulainen J. 1994. Lead and cadmium contents in pork, beef and chicken, and in pig and cow liver in Finland during 1991. Food Addit Contam. 11:415–426. Wagner HP. 1995. Determination of lead in beer using Zeeman background corrected graphite furnace atomic absorption spectrometry. J Am Soc Brew Chem. 53:141–144.