Analysis of perchlorate in baby food on Canadian (Ottawa) markets in 2009 and estimated dietary exposure.

In order to determine the baseline levels of perchlorate in major brands of baby food, 200 baby food products were collected from retail stores in Ottawa, Canada and analysed for perchlorate in 2010. The seven food groups tested were fruit, juices, vegetables, meat, yogurt, mixed (vegetable mixed with meat) and other (e.g. vegetable mixed with meat and cereal, cheese, egg,). Samples were extracted with a mixture of methanol and 1% acetic acid (4:1, v/v). Determination was conducted by stable isotope dilution ion chromatography tandem mass spectrometry (ID-IC-MS/MS). The complexity of different food matrices required additional method validation. The perchlorate levels in 46 samples were found to be lower than the quantification limit (0.2 ng g-1). The perchlorate levels in the other 154 baby food samples were also low; about 96.7% of the baby foods had perchlorate levels less than 10 ng g-1 (ranged from 0.2 to 22.4 ng g-1, median1.35 ng g-1); only 5 samples had perchlorate levels higher than 10 ng g-1. Dietary exposure to perchlorate from analysed baby food was conservatively estimated to range from 0.007 to 0.121 µg/kg bw/d based on the mean intake for children (1-5 years old).

Analysis of cocoa products for ochratoxin A and aflatoxins.

Eighty-five samples of cocoa products sampled in Canada were analysed for ochratoxin A (OTA) and aflatoxins in 2011-2012. Inclusion of the aflatoxins in this survey required additional method development. Chocolate was extracted with methanol-water plus NaCl, while for cocoa two successive extractions with methanol and methanol-water were made. Extracts were cleaned on an AflaOchra immunoaffinity column (IAC). Determination was by reversed phase high performance liquid chromatography (HPLC). Detection of the aflatoxins was with a post-column photochemical reactor and of OTA by fluorescence detection. Mean limits of quantification (LOQ) of chocolate and cocoa powders were 0.16 ng/g (OTA) and 0.07 ng/g (aflatoxin B1), respectively. Survey results showed that the incidences of OTA above the LOQ in natural cocoa were 15/15 (mean 1.17 ng/g), 20/21 for alkalized cocoa (mean 1.06 ng/g), 9/9 for baking chocolate (mean 0.49 ng/g), 20/20 for dark chocolate (mean 0.39 ng/g), 7/10 for milk chocolate (mean 0.19 ng/g), 5/5 for cocoa liquor (mean 0.43 ng/g), and 0/5 for cocoa butter. These results confirm our previous work with OTA. In the same samples, incidences of aflatoxin B1 above the LOQ were 14/15 for natural cocoa (mean 0.86 ng/g), 20/21 for alkalized cocoa (mean 0.37 ng/g), 7/9 for baking chocolate (mean 0.22 ng/g), 16/20 for dark chocolate (mean 0.19 ng/g), 7/10 for milk chocolate (mean 0.09 ng/g), 4/5 for cocoa liquor (mean 0.43 ng/g), and 0/5 for cocoa butter. Both aflatoxins and OTA were confirmed by HPLC-MS/MS when OTA or aflatoxin levels found were above 2 ng/g in cocoa.

Effect of cooking on concentrations of ß-estradiol and metabolites in model matrices and beef.

Because beef food products are generally cooked prior to consumption, the behavior of chemicals in these cooked foods is important in estimating human exposure. The heat stability of the natural estrogen ß-estradiol (ß-E2) and its metabolites α-estradiol (α-E2), estrone (E1), and several catechol estrogens was examined in heated vegetable oil and aqueous solutions. The chemicals were also incorporated into regular and extra lean ground beef and subjected to cooking. E1 and E2 were stable in aqueous solutions at 100°C, whereas the catechol estrogens exhibited first-order decay curves with half-lives of 2-10 min. Their stability improved to the same level as the other test chemicals when an antioxidant was added to the solution, suggesting that their disappearance was due to oxidation rather than thermal degradation. E1 and E2 were also stable in heated vegetable oil (160-180°C), whereas catechol estrogen decreased 30-50% over the 2 h duration of the experiments. Chemical losses from cooked beef appear to be related to the fat content of the beef, with greater losses occurring in regular ground beef (25-30%), compared to extra lean ground beef (5-20%). This study shows that cooking reduces but does not eliminate the potential for dietary exposure to growth promoters in ground beef.

Persistent organic pollutant residues in human fetal liver and placenta from Greater Montreal, Quebec: a longitudinal study from 1998 through 2006.

BACKGROUND: There is general concern that persistent organic pollutants (POPs) found in the environment, wildlife, food, water, house dust, human tissues, and fluids may alter normal human physiologic activities (e.g., fetal development, immune and endocrine systems). Although the levels of some POPs [polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCs)] in these matrices have decreased after their ban, others [polybrominated diphenyl ethers (PBDEs)] have increased in recent years. OBJECTIVE: To determine the longitudinal trend of specific POPs in human fetal tissues for risk assessment purposes. METHODS: We analyzed early to mid-gestation fetal liver (n = 52) and placental (n = 60) tissues, obtained after elective abortions during 1998-2006, for selected PBDEs, PCBs, and OCs using gas chromatography-mass spectroscopy. RESULTS: Total PBDEs in fetal liver increased over time (mean +/- SE: 1998, 284.4 +/- 229.8 ng/g lipid; 2006, 1,607.7 +/- 605.9; p < 0.03), whereas placental levels were generally lower, with no clear trend. Low levels of PCBs and OCs varied yearly, with no evident trend. The major analytes in 1998 were OCs (liver, 49%; placenta, 71%), whereas the major analytes in 2006 were PBDEs (liver, 89%; placenta, 98%). The 1998-2006 tissue PBDE congener profile is similar to that of DE-71, a commercial primarily pentabrominated diphenyl ether mixture manufactured in North America. CONCLUSIONS: Although commercial production of penta- and octa-brominated diphenyl ethers in North America was halted in 2004, their concentrations in fetal liver and placenta are now greater than the tissue burdens for the analyzed OCs and PCBs. Our findings also demonstrate that PBDEs accumulate within the fetal compartment at a very early stage in gestation.

Estimated dietary exposure to fluorinated compounds from traditional foods among Inuit in Nunavut, Canada.

Increasing evidence shows that persistent organic pollutants such as perfluorinated compounds (PFCs) are found in the Arctic ecosystem and their prevalence is causing human health concerns. The objective of this study was to estimate dietary exposure to PFCs among Inuit in northern Canada. Perfluorooctane sulfonate (PFOS), perfluorinated carboxylates (PFCA C(7)-C(11)) and fluorotelomer unsaturated carboxylic acids (6:2, 8:2 and 10:2 FTUCA) were measured in 68 traditional foods collected in Nunavut between 1997 and 1999. Total PFC concentrations were highest in caribou liver (mean+/-standard deviation; 6.2+/-5.5 ng g(-1)), ringed seal liver (minimum, maximum; 7.7, 10.2 ng g(-1)), polar bear meat (7.0 ng g(-1)), and beluga meat (minimum, maximum; 7.0, 5.8 ng g(-1)). Inuit food intake data from 24-h recalls conducted in Nunavut between 1997 and 1999 were used for the calculation of PFC exposure. Mean daily dietary exposure was calculated to range from 210 to 610 ng person(-1) (0.6-8.5 ng kg body weight(-1)) for 754 individuals. Dietary exposure to PFCs was statistically significantly higher in men in the 41-60 year age group (p<0.05) than younger men (<40 years old) and women from the same age group. Traditional foods contributed a higher percentage to PFC exposure than market foods in all age and gender groups. Caribou meat contributed 43-75% of daily PFC dietary exposure. Health risks associated with these estimated exposure levels are minimal based on current toxicological information available from animal feeding studies. However, it is important to monitor the concentrations of PFCs in key food items given that PFCA levels have been found to be increasing in the Canadian Arctic.

Cooking decreases observed perfluorinated compound concentrations in fish.

Dietary intake is a major route of exposure to perfluorinated compounds (PFCs). Although fish and seafood contribute significantly to total dietary exposure to these compounds, there is uncertainty with respect to the effect of cooking on PFC concentrations in these foods. Eighteen fish species purchased from markets in Toronto, Mississauga, and Ottawa, Canada were analyzed for perfluorooctanesulfonamide (PFOSAs)-based fluorochemicals and perfluorinated acids (PFAs) in raw and cooked (baked, boiled, fried) samples. Of 17 analytes, perfluorooctanesulfonic acid (PFOS) was detected most frequently; concentrations ranged from 0.21 to 1.68 ng/g ww in raw and cooked samples. PFOSAs were detected only in scallops at concentrations ranging from 0.20 ng/g ww to 0.76 ng/g ww. Total concentrations of PFAs in samples were 0.21 to 9.20 ng/g ww, respectively, consistent with previous studies. All cooking methods reduced PFA concentrations. Baking appeared to be the most effective cooking method; after baking samples for 15 min at 163 C (325 degrees F), PFAs were not detected in any of the samples. The margin of exposures (MOE) between the toxicological points of reference and the dietary intake of perfluorocarboxylates (PFCAs) and PFOS in fish and seafood muscle tissue were greater than 4 orders of magnitude. This indicates that reducing consumption of fish muscle tissue is not warranted on the basis of PFC exposure concerns at the reported levels of contamination, even for high fish consuming populations.

Organotin speciation and tissue distribution in rat dams, fetuses, and neonates following oral administration of tributyltin chloride.

Tributyltin (TBT) is a biocide that contaminates human foodstuffs, especially shellfish. TBT is an endocrine disrupter, producing imposex in several marine gastropods. Previous studies showed that oral dosing of rat dams with TBT chloride leads to abnormal fetal and postnatal development. In this study, the tissue distribution and speciation of organotins in tissues were examined in dams, fetuses, and neonates following dosing of rat dams commencing on gestational day (GD) 8 by oral gavage with TBT in olive oil at 0, 0.25, 2.5, or 10 mg/kg body weight (BW)/d. Dams' body weights were significantly reduced by the 10-mg/kg BW/d TBT treatment. At GD20, there were no significant effects of any TBT treatment on pup weights, litter size, sex ratio, or tissue weights. However, at postnatal day (PND) 6 and 12, neonatal pup weights were reduced by the 10-mg/kg BW/d TBT treatment but tissue weights were unaffected, except for the liver weight of female pups, which was reduced by the 10-mg/kg BW/d TBT treatment. Tissues harvested on GD20 and PND6 and PND12 were extracted for determination of organotins by gas chromatography-atomic emission detection (GC-AED). In most tissues, TBT and its metabolite dibutyltin (DBT) were evident but monobutyltin (MBT) was rarely measured above the detection limit. The livers and brains of fetuses contained TBT and DBT at levels that were approximately 50% of the equivalent tissues in the dams. Furthermore, these tissues appeared to preferentially absorb/retain organotins, since the concentrations were greater than were found for the total loading in whole pups. The placenta also contained relatively large quantities of TBT and DBT. Postnatally, the TBT levels in pups decreased markedly, a probable consequence of the extremely low levels of organotins in rat milk. However, DBT levels in pups livers and brains were maintained, probably due to metabolism of TBT to DBT. Similarly, while dams' spleens contained significant quantities of organotins, the pups' spleens contained smaller quantities, and these decreased rapidly between PND6 and PND12. These results show that organotins cross the placenta and accumulate in fetal tissues but that during lactation, the pups would receive minimal organotins through the milk and during this period, the levels of TBT in pups' tissues decreases rapidly. Consequently, fetuses would be at greater risk of the adverse effects of TBT, but due to the lack of transfer through milk, the risk would be reduced during the lactational period.

Determination of benzene in soft drinks and other beverages by isotope dilution headspace gas chromatography/mass spectrometry.

An automated, simple, and reproducible method was developed for the determination of benzene in soft drinks, based on isotope dilution headspace gas chromatography/mass spectrometry in the selected-ion monitoring mode. The method was used to assess benzene levels in samples of 124 soft drinks and beverages. Benzene was not detected in 60% of the 124 products. The average benzene levels in 6 products exceeded the Canadian maximum acceptable concentration of 5 microg/L for benzene in drinking water, and 2 of the 6 products had benzene levels above the World Health Organization guideline of 10 microg/L. The highest level of benzene, 23 microg/L, was found in a soft drink product specifically marketed to children.