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Land O’Lakes, Inc., Arden Hills, MN 55164
Corresponding author: P. A. Swearingen; e-mail: PASwearingen{at}landolakes.com.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSION DISCUSSIONCONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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Key Words: calcium lactate • liquid expulsion • starter culture • Cheddar cheese
Abbreviation key: S/M = salt in moisture
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSION DISCUSSIONCONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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The development of calcium lactate crystals on Cheddar cheese have been shown to be influenced by several factors (Pierce et al., 1973). Concentrations of calcium and lactate ions existing in cheese serum are very close to saturation and small increases in the concentration of either component could result in super saturation and crystallization. It is also theorized that milk citrate levels and the subsequent utilization of citrate by microorganisms may play a role in calcium lactate formation. Curd washing, curing, and storage temperature are also sited as other potential contributors to the defect. Morris et al. (1988) substantiated some of this information by defining that crystals were formed at a single nucleation site when concentration limits were reached.
More recent published work in this area (Thomas and Crow, 1983; Dybing et al., 1988; Johnson et al., 1990) also suggests that calcium lactate is formed when L (+)-lactate is converted into a racemic mixture of L(+)- and D(-)-lactate, the latter being much more prone to crystallization. The conversion of L(+)-lactate to D(-)-lactate is thought to be carried out by certain strains of lactobacilli and pediococci that are introduced into the cheese through cheese-milk and manufacturing.
The standard corrective actions to retard or prevent calcium lactate crystal formation on cheese has been to: 1) reduce the concentration of lactic acid in finished cheese, 2) reduce or eliminate undesirable lactobacilli or pediococci populations from the cheese manufacture process, 3) control storage temperature, and 4) vacuum package the cheese to minimize the airspace around the outer cheese surface where crystal formation takes place (Dybing et al., 1988; Olson and Johnson, 1989; Johnson et al., 1990; Johnson et al. 1990). Even when all of the above recommendations are incorporated into the manufacturing procedures for Cheddar cheese, calcium lactate crystal formation can still occur. This suggests another mechanism is involved in the development of the crystals.
Cheddar cheese is a matrix consisting of paracasein (in the form of a calcium-paracaseinate-calcium phosphate-complex), fat, water, lactic acid, minerals, and salt (sodium chloride). Physical-chemical properties of the paracasein such as water binding capacity and swelling are greatly affected by pH or acid level in cheese. Substantial work with mozzarella cheese (Guo et al., 1997; Kindstedt and Guo, 1998) has shown that cheese pH during manufacture and curing is vital to performance characteristics of that cheese. Their work has shown that as cheese pH is lowered, cheese calcium moves from the colloidal state (calcium paracaseinate-phosphate complex) to a soluble state (in serum). Increasing pH causes this reaction to reverse. Work by these and other researchers have also shown that as the calcium moves from the colloidal state to soluble state solubilization of paracasein occurs (Czulak et al., 1969; Guo et al, 1997; Curley et al., 1998). This process transforms cheese from a tough, rubbery, squeaky curd to a smooth, creamy, softer cheese.
In our studies, the influence of pH during manufacture and curing of Cheddar cheese was evaluated to understand its effects on the development of defects, including calcium lactate crystals and expulsion of free liquid from cheese in the retail package, a defect commonly referred to as weeping or wet. The cheese used in this study was manufactured commercially rather than in a pilot facility in order to better understand and define these 2 cheese defects and their incidence as they occur on a commercial scale.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSION DISCUSSIONCONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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). Starter was grown in external pH control starter media in bulk starter tanks. The inoculation target was 106 to 107 cfu/mL in cheese milk to assure proper fermentation of lactose.
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In our initial study, 4 vats of commercially manufactured Cheddar cheese were evaluated during early curing for pH and soluble and total calcium content. All vats were manufactured with the same starter culture group. Cheese curd was analyzed throughout the cheese-make, specifically at cook, pump-over, mill, block formation, 0.75 (18 h), 1, 7, 28, and 90 d. At cook and pump-over, the curd from each vat was sampled and drained, and a water extraction was performed immediately following draining. The filtrate was frozen and tested at a later time using the method described in the cheese chemistry section of this paper.
In the second study, blocks from 97 Cheddar cheese vats were sampled during curing at 3, 7, 14, 21, 28, 42 d and at 3, 4, 5, 6, 7, and 8 mo. A 30- to 35-g cheese sample was taken from Cheddar blocks using a Cheddar cheese block trier, model 8 M (Nelson-Jameson cat. no. 439-2005). To understand the effect of pH changes within the first week postmanufacture on appearance of calcium lactate and weeping defects during curing and shelf life, cheese was then selected based upon pH the change (increase or decrease [2 levels studied] from 3 to 7 d) to participate in a packaging and shelf-life study (Table 2). A total of 20 vats of cheese were selected and converted into packaged retail chunks and monitored for calcium lactate crystal formation and weeping defect in cheese throughout its shelf life.
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A paired t-test was used to determine whether the differences between sample populations (groups with and without the appearance of defect) were significant. Significance was determined at P < 0.05. Statistical analysis by t-test was performed using Microsoft Excel version 2002.
Cheese Chemistry
Cheese was examined for chemical composition including protein, fat, moisture, pH, and salt at 3 d postmanufacture. Protein and fat analysis were determined using Macro-Kjeldahl (N x 6.38) and Babcock methods (10). Cheese moistures were determined using a drying oven (102°C:IDF, 1982). Salt content was determined with a Corning Chloride Analyzer 926 (Corning, Medfield, MA). Cheese pH was measured with a Corning general-purpose combination electrode at ambient temperature.
Lactic acid and NPN were measured in cheese at 1 mo postmanufacture and at the end of the shelf-life study. D(-)- and L(+)- Lactic acid content in cheese was measured using a colorimetric method (Boehringer Mannheim Biochemical, Indianapolis, IN). The NPN method (AOAC International, 9991.21) was based on a 24% TCA precipitation of large and medium molecular weight peptides allowing for the measurement of small, soluble peptides and amino acids collected as a filtrate.
The total calcium content in cheeses was determined by atomic absorption spectrophotometry (12) during cheese manufacture and at 1 mo postmanufacture.
Soluble calcium was measured in cheese at 1 mo postmanufacture and at the beginning and end of the shelf-life studies. Samples for soluble calcium were prepared according to the method described by Kindstedt and Guo (1998). Modifications to their method were as follows: Water-extracts were prepared for all cheeses in the shelf life study at specified time intervals (beginning and end of shelf-life). Grated cheese (10 g) was mixed with 90 mL of deionized ambient water in an Osterizer Blender, model 6630 (Sunbeam Corporation) for 60 s on high speed. The mixture was immediately filtered through Whatman #4 paper. The filtrate was collected and analyzed by atomic absorption spectrophotometry to determine soluble calcium content.
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RESULTS AND DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSION DISCUSSIONCONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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, with each data point representing an average of 4 vats of cheese. The results of this study defined the need for additional test parameters in the second study where starter culture groups, lactic acid, and salt were also evaluated.
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). The average cheese pH was 5.01 at 7 d. After 7 d, soluble calcium levels changed very little through 3 mo, correlating well with little or no cheese pH change during that time. This is consistent with the work of Guo et al. (1997) that showed pH strongly influenced calcium-paracaseinate-complex causing calcium to move from the colloidal state to the soluble state (in serum) in cheese.
pH Profile in Cheddar During Curing
The pH of cheese was studied in order to understand the typical cheese pH pattern during curing for this manufacturing facility. Each of the 97 cheeses was evaluated for pH over 8 mo. At this particular facility, on average, cheese pH decreases from day of make and through early curing (less than one month). Figure 2 depicts the results of the pH assessment sorted by starter group used for the manufacture of the cheeses during this time period. On average, one starter culture blend (group 3) demonstrated a unique pH profile over the first month of curing compared with the other 4 starter culture blends used in this study. The pH pattern of group 3, differed from the others in that the rate of pH change slowed and the pH began to rise by the end of the first month. The other 4 culture blends were more dramatic in rate of cheese pH changes over the first month.
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shows the calcium lactate and weeping defect rate, as a percentage, observed in packaged cheeses at the end of shelf life by production day and vat. Varying levels of calcium lactate or weeping defects were apparent by the end of the retail shelf life of the cheese. These results showed that the pH change from 3 to 7 d had little affect on the presence or absence of either defect studied. However, when cheese was sorted by starter group used to manufacture the cheese, a high correlation was observed. Two to 6 vats of cheese were made with each starter group and only the use of starter group 3 resulted in defect free cheese.
Table 3 summarizes the defect rate by starter group for mild and sharp Cheddar. The mild Cheddar data shows that all culture groups, with the exception of group 3, developed some level of defect during their shelf life (42 to 69%). The same pattern was observed at the end of shelf life for the aged or sharp Cheddar cheese. The sharp Cheddar cheese data showed that the incidence of defects within each starter group varied, but most importantly, use of starter culture group 3 resulted again in cheese that did not manifest either calcium lactate formation or weeping. The defect rate by starter group for sharp Cheddar showed that all other culture groups developed some level of defect during their shelf life (74 to 100%).
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Several exceptions are noted in Table 2, where starter groups showed defect rates ranging from 0 to 100% within the same starter group. This may be explained by multiple strains, within a single starter group, growing disproportionately during preparation of starter batch, prior to use in cheese manufacture. This would lend to variability of strain populations within starter batches leading to strain population variation in cheese.
Cheese Chemistry: Ripening and Shelf Life in Retail Package
Calcium and soluble calcium.
Table 4 shows that the data collected for total calcium on both mild and sharp cheese at 6 mo and at the end of shelf life was not statistically different between the groups with and without the defects. Soluble calcium, however, was statistically significant in mild and sharp cheeses at the time of packaging between the defect and defect free groups. Cheese packaged as mild that would exhibit defects by the end of retail shelf life always demonstrated higher soluble calcium levels. While in aged cheese, by the end of the shelf life (14 mo after manufacture), when the greatest level of calcium lactate was present on the aged cheese surfaces, the soluble calcium level between defect and defect-free cheeses level was not statistically significant.
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). The level of L(+)-lactic acid did increase over time and by the end of shelf life, significant differences were observed between the defect and defect-free groups for both the mild (P < 0.0002) and aged (P < 0.0069) cheeses. This suggests that controlling the lactic acid levels at manufacture alone will not prevent calcium lactate crystal formation on cheese. However, it also suggests that as lactic acid levels increase over time, the propensity to develop the defects will increase. D(-)-Lactic acid was found to be less than 0.04% throughout this study, accounting for <1% of the total lactic acid in the cheese tested. The data show that microbial activity resulting in the conversion of L(+)-lactic acid to D(-)-lactic acid and the resulting reduced solubility did not play a part in the appearance of either calcium lactate or weeping defects. Variations in residual lactose levels in the cheeses made with different starter culture groups was not measured and, in retrospect, may have provided valuable information as to why lactic acid levels increased in some cheese over time.
Nonprotein nitrogen.
As expected, NPN levels increased during curing. This is a result of the generation of soluble peptides and amino acids from the degradation of primary protein and polypeptides during proteolysis. Neither the mild nor sharp cheeses showed any statistically significant differences between the defect and defect-free groups with respect to levels of NPN (Table 4). The significance of these data may be that protein degradation is not the first step in the release of soluble calcium into the serum.
Salt, moisture, salt in moisture.
The data shows that salt, moisture, and salt in moisture (S/M) are significant in the development of the cheese defects (Table 4). The average S/M for mild cheese exhibiting the defects was 4.19%, while the defect-free cheese was 4.55%. A similar pattern was also observed in the aged category, with the defect cheese having an average S/M of 4.22% and the defect-free cheese with an average of 4.55%. The S/M data suggest a possible control mechanism for preventing the defects. Examination of S/M data from individual vats of Cheddar shows that defect-free cheese (4.30 to 4.90%, mean 4.55%) overlaps across the entire range of cheese with the defect (3.81 to 4.85%, mean 4.22%). Furthermore, 6 of 14 defective vats had a S/M above 4.30%. This suggests that although statistically significant, controlling S/M in a range above 4.30% alone would not prevent the development of the defects.
Cheese pH.
The effect of cheese pH in our study is shown in Table 4. Cheese pH at mill did not correlate with the appearance of either calcium lactate or weeping in the mild or sharp cheese in this study (P > 0.05). The observed pH drop weeks and months after the cheese was manufactured corresponds well with increases in the level of lactic acid. In addition, soluble calcium levels were higher (P < 0.05) in cheese exhibiting defects (calcium lactate or weeping), which coincided with lower cheese pH (and higher lactic acid) as compared to defect-free cheese. Based upon our data, it appears it is not possible to control the weeping defect or the formation of calcium lactate by strictly controlling target pH values during the manufacturing of the cheese. Most importantly though, cheese pH drops below 5.00, postmanufacture, dramatically increases incidence of the defects, as does a pH drop below 4.96 within the first 6 wk postmanufacturing.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSION DISCUSSIONCONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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Cheese pH, within the first week (3 to 7 d), did not have an impact on the appearance of calcium lactate or weeping. In fact, many of the factors measured in early manufacturing and curing (less than 7 d) such as cheese pH at mill, lactic acid concentration, NPN, and calcium (total and soluble) did not correlate with the later appearance of either calcium lactate or liquid expulsion. Instead, surprisingly, starter culture used to manufacture the cheese was the most highly correlated measured factor in the study. It appeared that the levels of lactic acid produced by these organisms correlated with cheese pH. This would have affected calcium partitioning between intact cheese paracasein (colloidal) and the free-state or serum (soluble) as reported by Guo et al. (1997) and observed in the first study of this paper. In addition, an increase in soluble calcium, a reactant in the calcium lactate equilibrium reaction was observed in cheese serum.
The weeping defects observed in this research appear to be linked to the excessive decreases in cheese pH during curing and retail shelf life. Work by Hooydonk et al. (1988) has shown casein solvation (physically entrapped and nonsolvent water, in grams of H2O per gram of casein) decreases as the pH drops in renneted skim milk, particularly in the range of cheese manufacture and cure. The work showed that maximum water-holding capacity of renneted casein was at approximately pH 5.3. The excessive pH reductions observed in cheese likely resulted in a reduction in colloidal calcium beyond critical limits, that left paracasein (paracaseinate-complex) with a significant loss in ability to hold moisture.
The calcium lactate defect observed is thought to be related to the weeping defect. The serum that is expelled during weeping has a high concentration of calcium and lactic acid, well above the saturation point for L (+)-calcium lactate (3.44 g of calcium lactate per 100 gram of water at 4°C or 4.18 gram-calcium lactate per 100 gram of water at 10°C, both at pH 5.00 (Kubantseva, Hartel, and Swearingen, unpublished data) and if the optimal conditions are present, crystals will develop and grow. This would explain the difficulty is separating weeping and calcium lactate defects in cheeses, as noted in this paper.
Crystal formation will also be contingent upon the existence of nucleation sites. Rough surfaces created during cheese block cutting create crevices that give a lower energy requirement for crystal development to occur (Hartel, 2001). In addition, folds or ends of the cheese pieces, where no direct contact with packaging film occurs, are frequently the location where crystal form first (unpublished data).
The S/M phase was shown to be a possible control mechanism for preventing the defects discussed in this paper. Salt in the moisture will play some role in controlling starter culture fermentation activity and possibly the activity of the nonstarter bacteria. In addition, according to Guo et al. (1997), salt promotes the water-binding capability of paracasein, increasing a cheeses ability to hold moisture. This supports our findings where defect-free cheese had, on average, a higher salt level than defective cheese.
Starter cultures alone will not prevent or eliminate calcium lactate or weeping. Diligence with regard to good cheese manufacture practices will be critical, including minimizing residual lactose and controlling nonstarter lactic acid bacteria that readily drive pH reduction during curing. In addition, starter culture selection will likely be specific to each cheese manufacturer. Additional work should be completed to understand the specific phenotypic characteristics that starter cultures exhibit that contribute to the defects discussed in this study.
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CONCLUSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSION DISCUSSIONCONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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ACKNOWLEDGEMENTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSION DISCUSSIONCONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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Received for publication May 2, 2003. Accepted for publication September 5, 2003.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSION DISCUSSIONCONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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