Dietary exposure to acrylamide from cafeteria foods in ...

Research Article Received: 31 May 2016

Revised: 25 January 2017

Accepted article published: 14 March 2017

Published online in Wiley Online Library:

(wileyonlinelibrary.com) DOI 10.1002/jsfa.8314

Dietary exposure to acrylamide from cafeteria foods in Jeddah schools and associated risk assessment Mahmoud M El Tawila,a* Ahmed M Al-Ansari,a Amani A Alrasheedib and Abdulateef A Neamatallaha Abstract BACKGROUND: Acrylamide (AA) is a carcinogenic and genotoxic food contaminant produced at high temperatures in foods that are rich in carbohydrates. Foods sold in schools in Jeddah, Saudi Arabia, are among such carbohydrate-rich foods produced at high cooking temperatures. It is crucial to determine the importance of AA exposure with respect to cafeteria foods and assess the associated risks. RESULTS: The highest mean AA level was measured in chocolate pies (439 𝛍g kg−1 ), followed by custard pies (435 𝛍g kg−1 ) and cheese pies (432 𝛍g kg−1 ). The average and 95th percentile values of AA exposure were 0.51 and 1.17 [𝛍g kg−1 body weight (BW) school day−1 ]. The average exposure significantly decreased with an increase in age, from 0.65 (𝛍g kg−1 BW school day−1 ) in primary school students to 0.37 in secondary school students. Cheese and chocolate pies are the main contributors in AA intake. The contributions of cheese and chocolate pies to the average exposure among primary, middle and secondary school students were 23.1%, 24.7% and 29.4% and 16.9%, 12.1% and 11.9%, respectively. Other products with significant contributions included cheese sandwiches (10.8%, 8.9% and 12.7%), plain cookies (7.7%, 5.6% and 6.7%) and custard pies (7.7%, 4.8% and 8.9%). Other cafeteria products contributed to AA exposure at much lower percentages. CONCLUSION: The calculated margins of exposure (MOEs) for the average [356 and 614 for both benchmark dose lower confidence limit (BMDL) 0.18 and 0.31 mg kg−1 BW day−1 ] and 95th percentile AA exposure values (154 and 265 for both BMDL 0.18 and 0.31 mg kg−1 BW day−1 ) suggest that there is a health concern with respect to school-aged students. © 2017 Society of Chemical Industry Keywords: acrylamide; school cafeterias; HPLC; dietary exposure; risk assessment

INTRODUCTION Concerns about acrylamide (AA) levels in foodstuffs were first raised in 2002 at Stockholm University.1 AA forms during the cooking of starchy foods at temperatures higher than 120 ∘ C through the reaction of reducing sugars and free amino acids, such as the reduction of asparagine via the Maillard reaction.2 The level of AA produced depends on several major factors, including the processing temperature and time, the nature of the food matrix, the type and amount of carbohydrate, the layer thickness of the product, the amino acid content, the presence of additives and oils, and microwave usage.3 – 5 AA is ubiquitous in food, and more than 30% of a typical daily calorie intake comes from foods that contain AA.6 – 8 In a Western diet, the major foods contributing to AA exposure include potato chips, French fries, coffee, breadstuffs, and pastries and cookies (6–46%, 16–30%, 13–39%, 10–30% and 10–20%, respectively).4,9 However, AA exposure from potato chips in the Spanish population has been found to be moderate compared to other European countries.10 In 1994, the International Agency for Research on Cancer listed AA as ‘probably carcinogenic to humans’;11 this announcement served as the first warning that dietary exposure to AA could be J Sci Food Agric (2017)

a significant risk factor for cancer. The Joint Food and Agriculture Organization/World Heath Organization (WHO) Expert Committee on Food Additives (JECFA) has reported that the correlation between the intake of AA and biomarkers of exposure is very low, and a dose–response relationship for humans is unavailable.12 Additionally, a relationship between cancer and AA dietary exposure has not been positively confiemd, and the available studies indicate a lack of any increased risk for most types of cancer from exposure to AA.13 Therefore, the WHO has concluded that the risk associated with AA intake can be estimated through an assessment of dietary exposure based on a combination of food chemical concentration data and population exposure data.8,14

∗

Correspondience to: MM El Tawila, Department of Environmental Sciences, Faculty of Meteorology, Environment and Arid Land Agriculture, King Abdulaziz University, Jeddah, Saudi Arabia. E-mail: [email protected]; [email protected]

a Department of Environmental Sciences, Faculty of Meteorology, Environment and Arid Land Agriculture, King Abdulaziz University, Jeddah, Saudi Arabia b Food and Nutrition Department, Faculty of Home Economics, King Abdulaziz University, Jeddah, Saudi Arabia

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www.soci.org Because of the absence of epidemiological data and insufficient biomarker data, the dose–response relationship for the carcinogenic effects of AA has been determined based on data from animal studies. Consequently, the JECFA has proposed two different criteria for the benchmark dose lower confidence limit (BMDL)10 (the lower limit on the benchmark dose for a 10% response) for AA: the first being the development of Harderian gland tumors in mice [0.18 mg kg−1 body weight (BW) day−1 ] and the second being the induction of mammary tumors in rats (0.31 mg kg−1 BW day−1 ).12 The BMDL does not quantify the actual risk; instead, it is an estimate of the level of health concern. Therefore, an approach based on the margin of exposure (MOE), calculated as the ratio between the BMDL and the estimated dietary exposure, is typically used to perform a dietary AA risk assessment. The MOE approach is commonly used in risk assessments for many food chemicals, although it is based on animal data.15 – 18 AA exposure in children and adolescents is two to three times higher than that in adults because the younger population has a higher food intake per kg of BW compared to that of adults.19 Additionally, AA-rich foods, such as potato products, are more frequently consumed by children and adolescents than by the rest of the population.20 Very little information on AA exposure in Saudi Arabia is available. It was detected in several selected foods at Saudi local markets. The estimated average daily intake in this study was 0.57 μg kg−1 BW day−1 for 18–25-year-old girls.21 In another study, AA was detected in the range 3.4–950 μg kg−1 in some traditional Saudi foods. The calculated daily intake was 0.86 μg kg−1 BW day−1 for adults and 0.075 μg kg−1 BW day−1 for babies during the first 6 months after birth.22 In 1999, the Health Department of the Ministry of Education in Saudi Arabia agreed on a school cafeteria program with a consolidated list of cafeteria health requirements. Under this program, all school cafeterias under the Jeddah Governorate are currently operating through one food catering company. The food provided consists only of various bakery products and pies, which are known to be subject to AA formation during their production. Therefore, these products may be potential sources of exposure to AA, considering that the students eat them almost daily throughout the school year. Despite the availability of previous studies on AA in some Saudi food products.21,22 no study to date has documented AA levels in school cafeteria foods to which a large number of students are exposed. Therefore, the present study was conducted aiming to determine the importance of cafeteria foods in Jeddah city schools in causing AA exposure and to assess the risk associated with this exposure.

MATERIALS AND METHODS Food sampling Food samples (320 samples) were collected from schools cafeterias in the city of Jeddah in the Western Province of Saudi Arabia from September to November 2015, and interviews with students were conducted simultaneously. The collected samples included the following: 1 Pies, croissants and sandwiches (20 samples of each food type, 240 total samples): custard pies, plain pies, za’atar pies (thyme pies), labneh and za’atar pies (strained yogurt and thyme), apple pies, chocolate pies, cheese pies, cheese puffs, cheese

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sandwiches, cheese croissants, plain croissants and chocolate croissants. 2 Cookies and candy (20 samples of each food type, 80 total samples): popcorn, cookies, chocolates, and chocolate cookies. All foods were produced by a single supplier responsible for producing and supplying foods for governmental schools in Jeddah, Al Riyadh and Makkah, except for the cookies, chocolates and chocolate cookies, which were produced commercially by different companies. Chemicals and instrumentation AA standards and MAA were purchased from Sigma-Aldrich (Oakville, ON, Canada). All solvents were of high-performance liquid chromatography (HPLC) grade; acetonitrile, n-hexane and methanol were purchased from Fisher Scientific (Loughborough, UK). Water (HPLC grade) was purchased from Chem-Lab NV (Zedelgem, Belgium). The samples were cleaned and conditioned using Supel-Select HLB solid phase extraction (SPE) cartridges (bed weight 200 mg, volume 6 mL, product #54183-U; Sigma-Aldrich, St Louis, MO, USA), syringe filters (inner diameter 13 mm, pore size 0.2 mm) and cellulose acetate filters (inner diameter 35 mm, pore size 0.2 mm). Preparation of reference solutions AA standard stock solution (1 mg mL−1 ) was prepared by dissolving 50 mg of AA standard in 50 mL of water. MAA internal standard stock solution (1 mg mL−1 ) was prepared by dissolving 100 mg of MAA standard in 100 mL of water. All solutions were stored at 4 ∘ C, avoiding light for maximum stability, and working solutions were prepared daily by serial dilution in water. Sample preparation procedures A thoroughly homogenized sample was prepared by mixing equal weights of all 20 samples collected for each product. Three sub-samples of this homogenized sample were then used for AA determination. The samples were prepared using previously described methods, with a few modifications.23 – 25 In brief, 4 g of the homogenized sample was accurately weighed into each of three 50-mL centrifuge tubes. Each sample was spiked with 200 𝜇L of the MAA internal standard (1 mg mL−1 ) prior to the addition of 5 mL of hexane. The samples were shaken for 5 min using a vortex mixer (Fisher Scientific Co., Pittsburgh, PA, USA) for defatting. AA was extracted by shaking with 5 mL of water (HPLC grade) for 5 min using a vortex mixer, followed by filtration through filter paper. The hexane layer was then removed, and the defatting process was repeated. Subsequently, the lower layer was centrifuged for 10 min in a cooling centrifuge at 2688 g (Hermle Z383 K, HERMLE Labortechnik, Wehingen, Germany), the supernatant was filtered through a 0.2-mm syringe filter, and 1 mL of the filtrate was cleaned and conditioned using the SPE cartridge. Clean-up The SPE cartridge was conditioned with 5 mL of HPLC-grade methanol followed by 5 mL of HPLC-grade water. Following the conditioning step, 1 mL of the filtrate described previously was passed through the SPE cartridge. AA was then eluted with 1 mL of HPLC-grade water. The initial drops were discarded, and the filtrate was collected in 1.5-mL amber HPLC vials for chromatographic analysis.


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Dietary exposure to acrylamide from cafeteria foods Chromatographic conditions The acrylamide contents in the samples were determined by reverse phase-HPLC. The analysis was performed using an HPLC system (1200 Series; Agilent Technologies, Waldbronn, Germany) equipped with a ultraviolet–visible 190–600 nm diode array detector (DAD-G1315D) set at 195 nm. The system comprised a vacuum degasser (G1322A), a quaternary pump (G1311A), a temperature-controlled column oven (G1316A) set at 25 ∘ C and an auto sampler (G1329A). Separation was performed on a C18 column (Zorbax 5 μm ODS, 4.6 mm inner diameter × 250 mm; Agilent Technologies). The operating conditions were: isocratic mobile phase of water and acetonitrile (95:5 v/v), with all solutions being degassed in an ultrasonic bath (HB-4818 T; Kendal, Guangdong, China) for 10 min and filtered through 0.2-mm cellulose acetate filters before use. The flow rate was set at 0.7 mL min−1 ; injection volume, 20 𝜇L; column temperature 25 ∘ C. Peak identification was based on the retention time, by a comparison of the ratio of ultraviolet spectra with that of a standard AA. The obtained data were processed using the ChemStation Manager (revision B.04.02 SP1; Agilent Technologies). Method validation The analytical method was validated by determining the linearity, limit of detection (LOD), limit of quantification (LOQ) and recovery percentage. The linearity of the standard curve was expressed in terms of the correlation coefficient (r) for the formula y = mx + b (m = 150.7 and b = 5.1) and was found to be satisfactory (r = 0.9995) for AA concentrations in the range 0.05–10 μg mL−1 . The LOD and LOQ were determined based on the SDs of the response and the slope (r). The ratio of the SD of the y intercepts of the regression lines to the slopes was multiplied by 3.3 to obtain the LOD and by 10 to obtain the LOQ. The slope values were calculated from the linearity experiments. The LOD and LOQ values of the method were 3.9 and 11.9 μg kg−1 , respectively. The accuracy of the method was determined based on recovery experiments with MAA as the internal standard. The mean recovery was found to be 94%, which is a recovery percentage that is generally accepted for AA determination in food products.

www.soci.org clothing by subtracting 1.2 and 0.8 kg from the BW of boys and girls, respectively.26 The exposure of students to AA was assessed by combining the analytical AA results with the data on the individual consumption of the cafeteria foods. Exposure as a result of cafeteria foods was calculated using the formula: ∑ Qik × Cik Ei = BWi × 2 where E i is the dietary AA exposure of student i (μg kg−1 BW sd−1 ), Qik is the amount of food item k consumed by student i over two school days, C ik is the AA concentration in food item k (μg kg−1 ), BWi is the BW of student i (kg) and Σ denotes the sum over all food items consumed by student i among the cafeteria foods. Thus, the exposure calculated based on two school days of cafeteria food consumption) was divided by 2 to obtain the daily AA exposure. Risk assessment of AA exposure from cafeteria foods MOE values were calculated by comparing the mean and 95th percentile values of AA exposure against BMDL10 values (0.18 mg kg−1 BW day−1 for the development of Harderian gland tumors in mice and 0.31 mg kg−1 BW day−1 for the induction of mammary tumors in rats).12,27,28 Statistical analysis Descriptive statistics were calculated for the AA contamination of the cafeteria foods, the dietary AA exposure of the students and selected percentiles (P10, P50 and P95) of the studied groups. The dietary intake of AA did not follow a normal distribution; therefore, a Mann–Whitney U-test was used to determine the significance of the difference in AA exposure between boys and girls. A Kruskal–Wallis test was used to test the significance of the differences among the three educational levels, where a value of 𝛼 = 0.05 was considered to indicate statistical significance.29 SPSS, version 22 (IBM Corp., Armonk, NY, USA) was used for the statistical analysis.30

RESULTS AND DISCUSSION Dietary AA exposure assessment A cross-sectional descriptive study was conducted over 3 months from October to November 2015. The participants enrolled in the study were male (n = 587) and female (n = 536) students who were selected from primary, middle and secondary schools. The required permissions for the study were obtained from the Ministry of Education. A multistage, stratified sampling technique was used to recruit the study sample. The study included primary school (nine schools) classes of the three highest levels (levels four, five and six) and classes of all three levels in both middle (eight schools) and secondary schools (eight schools). A systematic random sampling procedure was used to select schools from the official list of all Jeddah city sectors. For all schools enrolled in the present study, 15 students each from one class of each level were randomly selected. A food frequency questionnaire (FFQ) was administered to investigate the students’ consumption of food from the school cafeterias on school days (sd). All foods available in the school cafeteria were recorded in the FFQ. The BW was measured for all selected students to the nearest ‘100 g’ with the student in light clothes, without shoes. The scale was calibrated daily before weighing any student to assure the zero. The BW was adjusted for J Sci Food Agric (2017)

AA in school cafeteria foods Cafeteria foods are the main source of breakfast meals for students at all stages of their education in Jeddah schools, with 66% of students purchasing foods from cafeterias once per day and 14% doing so two or more times per day.31 The types of foods sold in Jeddah schools are various bakery products, such as pies and sandwiches, which have been identified in many previous studies as being important sources of AA. Therefore, the consumption of these products on a daily basis throughout the school year should be regarded as an important and continuous source of AA exposure. All cafeteria foods offered in Jeddah schools were found to contain levels of AA higher than the LOD and LOQ. This is because all of these products are carbohydrate-rich foods that are prepared at high temperatures, which leads to AA formation. It is also important to note that a single supplier produces all of the investigated cafeteria products and uses almost the same ingredients and cooking conditions for each product type. The producing company is a leader company in the catering and food industry in Saudi Arabia. Its products and services are offered to a diversified range of public and private customers, such as hospitals, universities, schools, social centers, military and security sectors.



www.soci.org Among the 16 investigated cafeteria products, the highest mean AA levels were found in chocolate pies (439 μg kg−1 ), custard pies (435 μg kg−1 ) and cheese pies (432 μg kg−1 ) (Table 1). The detected levels of AA were consistent with the levels measured for biscuits and cookies in the USA (169–518 μg kg−1 ),12 and, to a lesser extent, the results for oven-baked confectionary products sold in Italian markets (126–385 μg kg−1 ).32 The AA levels in the chocolate cookies (183 μg kg−1 ) offered in Jeddah schools were found to be slightly higher than the levels measured in similar products in a French total diet study (139 μg kg−1 ).33 In general, AA formation in chocolate products is highly variable, ranging from non-detectable to approximately 900 μg kg−1 .34 This is attributed to the type of cocoa beans used in chocolate production, as well as to the roasting process time and temperature used to develop the characteristic chocolate flavor.35 Furthermore, the variations in AA concentration among samples of the same type or from the same group of foods that have appeared in many studies have been attributed to variations in heating temperature and time, different carbohydrate types and amounts, different layer thicknesses of the products, the presence of different amino acids and other additives, and the different types of fillings used in some products.3 – 5 Exposure assessment Table 2 summarizes the characteristics of AA exposure caused by cafeteria foods. The overall mean and 95th percentile values for the AA exposure of school students were found to be 0.51 and 1.17 μg kg−1 BW sd−1 , respectively. This dietary exposure represents only the exposure from the consumption of cafeteria foods during the school day. However, this intake is similar to or even higher than the estimated total daily AA intake in several other countries. For example, in a Chinese total diet study, the mean and 95th percentile dietary intake values were found to be 0.286 and 0.490 μg kg−1 BW sd−1 , respectively. In France, the average dietary intakes have been found to be 0.45 and 0.69 μg kg−1 BW day−1 for adults and children, respectively, and the 95th percentile values are 1.71 and 1.8 μg kg−1 BW day−1 , respectively.33 In Canada, the mean and 95th percentile daily intake values are 0.58 and 2.19 μg kg−1 BW day−1 , respectively.36 According to data gathered by the JECFA, the estimates of mean AA intake among 17 countries range from 0.3 to 2.0 μg kg−1 BW day−1 , and the estimates of AA exposure in children are two to three times higher than those for adults.37 Meanwhile, the JECFA12 has estimated the mean dietary exposure to AA in the general adult population to lie in the range 0.2–1.0 μg kg−1 BW day−1 and the highest intake is estimated to be 0.6–1.8 μg kg−1 BW day−1 . In two previous studies, the average dietary exposure in Saudi Arabia has been estimated to be 0.57 and 0.86 μg kg−1 BW day−1 . However, both studies were conducted with a limited number of participants (100 and 50 subjects, respectively) and one study estimated exposures only in the female population.21,22 In the present study, dietary exposure was found to be higher in the younger (primary school) students compared to older students (in middle and secondary schools). Average AA exposure decreased significantly with increasing age (P < 0.05), from 0.65 μg kg−1 BW sd−1 in the youngest group to 0.37 μg kg−1 BW sd−1 in the oldest group. The 95th percentile values of AA intake also decreased with increasing age, from 1.40 in primary school students to 1.04 and 0.86 in middle and secondary school students, respectively. The same trend was observed in the P10, P50 and average exposure values (Table 2). This finding is similar to those obtained in several studies, such


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as in southern Poland, where AA exposure was found to decrease from 1.51 μg kg−1 BW day−1 in the youngest group (6–12 years) to 0.67 μg kg−1 BW day−1 in the oldest group (42–60 years).27,38,39 A significant difference (P < 0.05) between boys and girls in exposure to AA from the consumption of school cafeteria foods was found only in students at the primary school level (Table 2). The contribution of each of the cafeteria products to the mean dietary exposure to AA is provided in Table 3. Cheese pies, chocolate pies, cheese sandwiches, custard pies and plain cookies represent the major sources of AA exposure among the school cafeteria foods that were investigated. Compared to other products, these products were the most preferred and most frequently consumed by students at all educational levels. These five products represent the majority of the total AA exposure (66.2%, 56.1% and 69.6% for primary, middle and secondary school students, respectively). The high contribution of these products can be attributed to their high levels of AA contamination or their high consumption rates, or both. The differences between countries in terms of the foods that contribute most significantly to total dietary AA exposure can be primarily attributed to differences in consumption habits.33 In Poland, bakery products are the main source of AA because of the high consumption of bread by the Polish population (60 kg per inhabitant per year).27 Similarly, in Germany, where 83 kg of bread is consumed per inhabitant per year, a significant proportion of the total intake of AA originates from the ingestion of bread and other bakery products (18–46%).40 For most other countries, the foods that represent the largest contributions to dietary AA exposure are French fries, potato chips, breadstuffs, and pastries and cookies (10–60%, 10–22%, 13–34% and 10–15%, respectively).27,41,42 French fries and other potato products are the most important contributors to AA intake in many countries, such as in France (45% for adults and 61% for children)33 and the USA (where potato chips are the main contributor),37 because of their particularly high levels of both consumption and AA contamination. Fortunately, the consolidated list of health requirements for school cafeterias issued by the School Health Department in Saudi Arabia prohibits the provision of French fries and potato chips as part of the meals provided in school cafeterias; otherwise, significantly higher levels of AA intake might be expected. Risk assessment Given that AA is a possible genotoxic carcinogen, the MOE approach may provide an idea of the risks associated with its presence in food.18 The MOE approach remains the most common method of risk characterization with respect to AA and all other food chemicals, despite some uncertainties derived from the use of data from rodents to assess the dose–response curve and the lack of human external or internal exposure studies to confirm its validity.17 The MOEs calculated for the overall mean AA exposure were 356 and 614 for the two BMDL10 values (0.18 and 0.31 mg kg−1 BW day−1 , respectively) (Table 4). The obtained MOE values are close to those suggested by the JECFA to indicate an AA health concern (range 45–310). The EFSA/WHO considers a public health issue to exist, requiring efforts to reduce exposure, when the MOE value is lower than 10,000 based on a given BMDL10 .16 For the different educational levels, the MOEs calculated for mean AA exposure increased with age from 277 to 486 for the BMDL10 value of 0.18 mg kg−1 BW day−1 and from 477 to 838 for 0.31 mg kg−1 BW day−1 . The same trend was also observed for the 95th percentile of exposure, for which the MOEs increased



Dietary exposure to acrylamide from cafeteria foods

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Table 1. Acrylamide levels (μg kg−1 ) in school Cafeteria foods in Jeddah city Concentration (μg kg−1 ) Food groups

Number of samples

Pies, sandwiches and croissants Custard pies Plain pies Za’ataar piesa Labneh and za’ataar piesb Apple pies Chocolate pies Cheese pies Cheese Puffs Cheese croissant Plain croissant Chocolate Croissant Cheese sandwiches Cookies and candies Plain cookies Chocolates Popcorn Chocolate cookies

Mean ± SD

Minimum concentration

Maximum concentration

20 20 20 20 20 20 20 20 20 20 20 20

435 ± 93 169 ± 89 308 ± 36 200 ± 54 186 ± 31 439 ± 155 432 ± 71 197 ± 89 141 ± 47 263 ± 91 364 ± 125 236 ± 57

367 71 258 141 153 257 323 100 98 204 257 188

540 296 347 247 200 638 491 383 186 368 542 338

20 20 20 20

141 ± 43 138 ± 63 150 ± 68 183 ± 34

90 71 74 138

182 208 235 200

a Thyme pies. b Strained yogurt and thyme.

Table 2. Mean acrylamide exposure (μg kg−1 BW sd−1 ) from cafeteria foods among males and females of different age groups

Educational level (age group) Primary Age (9–11 years) Middle Age (12–14 years) Secondary Age (15–17 years) Total Age (9–17 years)

Sex Boys Girls Boys and girls Boys Girls Boys and girls Boys Girls Boys and girls Boys Girls Boys and girls

n 227 182 409 135 172 307 225 182 407 587 536 1123

Mean 0.69 0.57 0.65 0.47 0.53 0.50 0.36 0.40 0.37 0.51 0.50 0.51

P10

P50

P95a

0.28 0.06 0.23 0.05 0.10 0.09 0.06 0.02 0.04 0.10 0.06 0.05

0.63 0.49 0.59 0.45 0.50 0.47 0.32 0.29 0.31 0.47 0.43 0.45

1.33 1.54 1.40 0.98 1.11 1.04 0.80 1.01 0.86 1.15 1.25 1.17

Maximum 2.47 2.28 2.47 1.33 1.87 1.87 1.16 4.18 4.18 2.47 4.18 4.18

Significance between boys and girls (Mann–Whitney U-test) 0.000b

Significance between educational levels (Kruskal–Wallis test) 0.000b

0.198

0.801

0.086

a

High exposure. Significantly different at P < 0.05. Percentiles (P10, P50 and P95) of intake for different educational levels, sex and total population were calculated for all respondents of each group.

b

with age from 129 to 209 and from 221 to 360 for the two BMDL values, respectively. For the high-consumption group, the AA exposure exceeds the average exposure by more than three-fold (mean exposure 1.17–4.18 μg kg−1 BW sd−1 ); therefore, the calculated MOEs for the high-consumption group are lower (43–154 and 74–265 for BMDL10 values of 0.18 and 0.31 mg kg−1 BW day−1 , respectively). The low MOE values obtained for exposure to cafeteria foods indicate that AA is an important issue of concern for school students. This means that the general exposure levels of AA will be higher and potential risks will increase, especially with the J Sci Food Agric (2017)

high rate of consumption of carbohydrate-rich foods by the Saudi population. In a 24-h food recall study, the mean carbohydrate intakes for rural (Dawadami) and urban (Riyadh city) students were 209 g day−1 and 238 g day−1 , respectively. It was also found that 45.3% and 48.3% of students, respectively, consumed bread and cereal products seven or more times a week, knowing that, the school cafeteria program is not applied in Dawadami and all rural areas.43 Based on all of the above, certain actions should be taken to reduce AA exposure from cafeteria foods. Examples of such actions include mitigation studies conducted in Switzerland, Belgium and



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Table 3. Contribution of each cafeteria food to the mean acrylamide exposure (μg kg−1 BW sd−1 ) among school students Primary schools (9–11 years)

Middle schools (12–14 years)

Percentilesa

Percentiles

Food item

Mean P10

P50

P95

Custard pies Plain pies Za’ataar pies Labneh and Za’ataar pies Apple pies Chocolate pies Cheese pies Cheese Puffs Cheese croissant Plain croissant Chocolate Croissant Cheese sandwiches Plain cookies Chocolates Popcorn Chocolate cookies Total

0.05 0.02 0.03 0.01 0.01 0.11 0.15 0.02 0.01 0.02 0.02 0.07 0.05 0.02 0.03 0.03 0.65

0.46 0.08 0.16 0.00 0.01 0.21 0.20 0.09 0.07 0.11 0.16 0.14 0.05 0.03 0.05 0.05 0.63

1.10 0.13 0.41 0.00 0.14 0.33 0.30 0.12 0.09 0.16 0.21 0.20 0.07 0.05 0.07 0.06 1.40

0.19 0.06 0.11 0.00 0.06 0.14 0.12 0.06 0.04 0.06 0.11 0.09 0.03 0.02 0.03 0.03 0.19

Secondary schools (15–17 years)

Contribution % 7.7 3.1 4.6 1.5 1.5 16.9 23.1 3.1 1.5 3.1 3.1 10.8 7.7 3.1 4.6 4.6 100.0

Mean P10

P50

P95

0.024 0.023 0.022 0.002 0.008 0.061 0.124 0.025 0.019 0.024 0.034 0.045 0.028 0.014 0.025 0.022 0.503

0.30 0.05 0.11 0.00 0.08 0.16 0.16 0.07 0.05 0.09 0.12 0.11 0.03 0.02 0.03 0.03 0.47

0.65 0.07 0.52 0.13 0.21 0.47 0.57 0.13 0.07 0.22 0.30 0.34 0.07 0.04 0.05 0.06 1.00

0.15 0.04 0.08 0.00 0.05 0.12 0.11 0.05 0.04 0.06 0.09 0.08 0.03 0.02 0.02 0.02 0.09

Percentiles Contribution % 4.8 4.6 4.4 0.4 1.6 12.1 24.7 5.0 3.8 4.8 6.8 8.9 5.6 2.8 5.0 4.4 100.0

Mean P10

P50

P95

0.033 0.014 0.009 0.006 0.003 0.044 0.109 0.013 0.014 0.012 0.006 0.047 0.025 0.011 0.009 0.016 0.371

0.11 0.05 0.09 0.00 0.06 0.14 0.13 0.06 0.05 0.08 0.11 0.10 0.04 0.02 0.03 0.03 0.31

0.18 0.07 0.11 0.00 0.08 0.23 0.18 0.08 0.06 0.10 0.14 0.13 0.04 0.03 0.04 0.04 0.86

0.08 0.04 0.07 0.00 0.05 0.11 0.10 0.05 0.03 0.06 0.09 0.07 0.03 0.02 0.02 0.02 0.04

Contribution % 8.9 3.8 2.4 1.6 0.8 11.9 29.4 3.5 3.8 3.2 1.6 12.7 6.7 3.0 2.4 4.3 8.9

Percentiles (P10, P50 and P95) for each food were calculated for consumers of each food only. However, the total corresponds to all respondents.

Table 4. Estimation of margin of exposure (MOE) for mean and 95th percentile of acrylamide dietary exposure Primary schools (9–11 years)

Middle schools (12–14 years)

Secondary schools (15–17 years)

Jeddah schools (9–17 years)

Educational level (age)

Mean

P95a

Mean

P95a

Mean

P95a

Mean

P95a

Dietary exposure (μg kg−1 BW sd−1 ) MOE (BMDL10 = 0.18 mg kg−1 BW day−1 )b MOE (BMDL10 = 0.31 mg kg−1 BW day−1 )b

0.65 277 477

1.40 129 221

0.503 358 616

1.00 180 310

0.37 486 838

0.86 209 360

0.505 356 614

1.17 154 265

a b

95th percentile (high exposure). BMDL10 defined for carcinogenic effects.12

Lithuania, as well as a dietary modification study conducted in Finland, which led to significant decreases in AA content in many products, including potato products, bread and rolls, breakfast cereals, chocolate and biscuits, in these countries.18,44 – 46 Recently, guidelines for manufacturers to reduce AA in foods have been established by the US Department of Health and Human Services in collaboration with the Food and Drug Administration and the Center for Food Safety and Applied Nutrition. Detailed guidelines for reducing AA formation in all steps of the production process, from raw materials to the final processed products, have been formulated.47

CONCLUSIONS According to the results of the present study, the levels of AA in cafeteria foods in Jeddah city schools, the dietary exposure (0.505 μg kg−1 BW sd−1 ) and the calculated MOE values (356 and 614 for both BMDL 0.18 and 0.31 mg kg−1 BW day−1 ) indicate that such AA exposure should be considered an important health issue. A risk management strategy is required, and efforts should be made to reduce the number of bakery products and pies


consumed daily by students. Additionally, the school cafeteria food supplier should take advantage of the mitigation strategies suggested in several other countries to reduce AA formation in their products.

ACKNOWLEDGEMENTS This project was funded by the Deanship of Scientific Research (DSR) at King Abdulaziz University, Jeddah, under grant no (G-383-155-36). The authors, therefore, acknowledge with thanks DSR for technical and financial support.

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