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- Selin, Erica, et al.
(author)
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Food contact materials: an effect-based evaluation of the presence of hazardous chemicals in paper and cardboard packaging
- 2021
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In: Food Additives & Contaminants. - : Informa UK Limited. - 1944-0049 .- 1944-0057. ; 38:9, s. 1594-1607
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Journal article (peer-reviewed)abstract
- Food contact materials (FCMs) can contain hazardous chemicals that may have the potential to migrate into food and pose a health hazard for humans.Previous studies have mainly focused on plastic materials, while data on packaging materials made from paper and cardboard are limited.We used a panel of cell-based bioassays to investigate the presence and impact of bioactive chemicals on human relevant endpoints like oxidative stress, genotoxicity, inflammation, xenobiotic metabolism and endocrine system effects in extracts made from paper and cardboard.In total, 23 methanol extracts of commonly used paper and cardboard available on the Swedish market were extracted as a whole product using methanol to retrieve polar substances, and tested at concentrations 0.3–10 mg/mL and 0.2–6 mg/mL. At the highest concentration bioactivities were observed in a high proportion of the samples: oxidative stress (52%), genotoxicity (100%), xenobiotic metabolism (74%), antiandrogenic- (52%) and antioestrogenic receptor (39%).Packages of potential concern included cake/pastry boxes/mats, boxes for infant formula/skimmed milk, pizza boxes, pizza slice trays and bag of cookies.It should be noted that the extraction for packages like cake/pastry boxes can be considered exaggerated, as the exposure usually is shorter. It can be hypothesised that the observed responses may be explained by inks, coatings, contaminants and/or naturally occurring compounds within the material.To summarise, an effect-based approach enables hazard identification of chemicals within FCMs, which is a valuable tool for ensuring safe use of FCMs.
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| 3. |
- Oskarsson, Agneta, et al.
(author)
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Short communication: Staphylococcus aureus infection modulates expression of drug transporters and inflammatory biomarkers in mouse mammary gland
- 2017
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In: Journal of Dairy Science. - : American Dairy Science Association. - 0022-0302 .- 1525-3198. ; 100, s. 2375-2380
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Journal article (peer-reviewed)abstract
- Mastitis is the most common disease in dairy herds worldwide and is often caused by Staphylococcus aureus. Little is known about the effect of mastitis on transporters in the mammary gland and the effect on transporter-mediated secretion of drugs into milk. We studied gene expressions of ATP-binding cassette and solute carrier transporters in S. aureus-infected mammary glands of mice. On d 7 of lactation, NMRI mice were inoculated with 1,000 cfu of S. aureus in 2 mammary glands and with a saline vehicle in 2 control glands. Gene expression of the transporters, Bcrp, Mdr1, Mrp1, Oatp1a5, Octn1, and Oct1, and of Csn2, the gene encoding O-casein, were determined in mammary glands at 72 h after treatment. As biomarkers of the inflammatory response gene, expressions of the cytokines Il6, Tnf alpha, and the chemokine Cxc12 were measured. Despite a high individual variation between the 6 animals, some characteristic patterns were evident. The 3 inflammatory biomarkers were upregulated in all animals; Csn2 was downregulated compared with controls in all animals, although not statistically significantly. Both Mrp1 and Oatp1a5 were statistically significantly upregulated and Bcrp was downregulated. Gene expression of Bcrp followed the expression of Csn2 in each of the animals, indicating a possible co-regulation. The findings demonstrate that S. aureus infection has an effect on expression of drug transporters in the mammary gland, which may affect secretion of drugs into milk and efficacy of drug therapy.
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| 4. |
- Selin, Erica, et al.
(author)
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Hazardous chemicals in non‑polar extracts from paper and cardboard food packaging: an effect‑based evaluation
- 2022
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In: Environmental Sciences Europe. - Stockholm : IVL Svenska Miljöinstitutet AB. - 2190-4707 .- 2190-4715. ; 34:1
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Journal article (peer-reviewed)abstract
- Background: Food contact articles are used in our everyday life and information regarding the potential health hazards of migrating chemicals for humans is scarce. In this study, an effect-based evaluation of non-polar extracts of food contact articles made of paper and board was conducted with a panel of eight bioassay endpoints. These, health-relevant endpoints, included oxidative stress, inflammation, genotoxicity, xenobiotic metabolism and hormone receptor effects.Results: In total, 62 food contact articles were pooled into 19 groups, in which articles intended to be used for similar types of food item(s) were pooled, and extracted with acetone:n-hexane (1:4). These were then tested in the effectbased bioassays. Bioactivities were detected for multiple materials in six out of eight assays, the two assays showing no effects were NFκB and androgen receptor agonistic response. In essence, the detection rates of the tested non-polar extracts were 72% for antagonistic effects on the estrogen receptor, 72% for antagonistic effects on the androgen receptor, 47% for oxidative stress, 28% for agonistic effects on the estrogen receptor and 33% for genotoxicity. The bioequivalent concentrations ranges in extracts of 10 mg food contact article/mL cell culture media were: for oxidative stress from 2.45 to 5.64 μM tBHQ equivalents, estrogen receptor agonistic activity from 1.66 to 6.33 ρM estradiol equivalents, estrogen receptor antagonistic activity from 1.21 × 10–3 to 4.20 × 10–3 μM raloxifene equivalents and androgen antagonistic activity 0.08–0.46 μM hydroxyflutamide equivalents.The extracts that were bioactive in multiple assays were: baking moulds, boxes for popcorn, infant formula/skimmed milk, porridge/flour mixes, pizza, fries’ and hamburgers as well as packages for frozen food.Conclusion: Non-polar extracts of food contact articles contain compounds that can activate molecular initiating events in toxicity pathways of high relevance to human health. These events included endocrine-disruptive activities, oxidative stress and genotoxicity. Effect-based methods proved to be a valuable tool for evaluating food package articles, as they can detect potentially hazardous effects of both known and unknown chemicals as well as potentialcocktail effects.
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| 5. |
- Oskarsson, Agneta, et al.
(author)
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Acetaminophen Increases Aldosterone Secretion While Suppressing Cortisol and Androgens : A Possible Link to Increased Risk of Hypertension
- 2016
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In: American Journal of Hypertension. - : Oxford University Press (OUP). - 0895-7061 .- 1941-7225 .- 1879-1905. ; 29:10, s. 1158-1164
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Journal article (peer-reviewed)abstract
- Acetaminophen (paracetamol) is a widely used analgesic and antipyretic drug. Potential side effects are of public health concern, and liver toxicity from acute overdose is well known. More recently, a regular use of acetaminophen has been associated with an increased risk of hypertension. We investigated effects of acetaminophen on steroidogenesis as a possible mechanism for the hypertensive action by using the human adrenocortical cell line, H295R. Cells were treated with 0.1, 0.5, and 1mM of acetaminophen for 24 hours, and secretion of steroids and gene expression of key steps in the steroidogenesis were investigated. Progesterone and aldosterone secretion were increased dose dependently, while secretion of 17 alpha-OH-progesterone and cortisol as well as dehydroepiandrosterone and androstenedione was decreased. CYP17 alpha-hydroxylase activity, assessed by the ratio 17 alpha-OH-progesterone/progesterone, and CYP17-lyase activity, assessed by the ratio androstenedione/17 alpha-OH-progesterone, were both dose-dependently decreased by acetaminophen. No effects were revealed on cell viability. Treatment of cells with 0.5mM of acetaminophen did not cause any effects on the expression of 10 genes in the steroidogenic pathways. The pattern of steroid secretion caused by acetaminophen can be explained by inhibition of CYP17A1 enzyme activity. A decreased secretion of glucocorticoids and androgens, as demonstrated by acetaminophen, would, in an in vivo situation, induce adrenocorticotropic hormone release via negative feedback in the hypothalamic-pituitary-adrenal axis and result in an upregulation of aldosterone secretion. Our results suggest a novel possible mechanism for acetaminophen-induced hypertension, which needs to be further elucidated in clinical investigations.
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| 7. |
- Oskarsson, Agneta
(author)
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Chapter 60. Vanadium
- 2014
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In: Handbook on the Toxicology of Metals. - 9780444594532 ; , s. 1347-1367
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Book chapter (other academic/artistic)abstract
- Absorption of vanadium from the gastrointestinal tract is poor, not exceeding 2% in humans. Soluble compounds of vanadium are absorbed to a considerable extent after inhalation and concentrated in the lung, but available information is not adequate for a reliable estimation of dose-response relationships. Absorbed vanadium is widely distributed in the body. In animals, the highest values are found in the bone, kidney, liver, and spleen. Bone maintains essentially unchanged levels for several weeks. Low concentrations have been detected in the brain, and in animal placenta and testes. Urine is the predominant route of excretion of absorbed vanadium. Animal and human data indicate that excretion occurs in at least two phases. A three-compartment model for elimination is described in humans, with half-times after intravenous injection of 1.2h, 26h, and 10-12 days. Vanadium is essential for certain bacteria and microorganisms. Some reports suggest that vanadium is essential for mammals, but no biochemical function has been defined in humans. The total dietary intake is estimated to be 6-30μg/day, and in some regions up to 50μg/day. The use of vanadium as a supplement for athletes and body builders has been reported. Point-of-contact non-neoplastic and neoplastic effects in experimental animals occur in the respiratory tract. Systemic effects have been observed in the liver, kidney, nervous system, cardiovascular system, and blood-forming organs. Metabolic effects include interference with the biosynthesis of cystine and cholesterol, depression and stimulation of phospholipid synthesis, and, at higher concentrations, inhibition of serotonin oxidation. Vanadate has been shown to inhibit sodium/potassium-transporting ATPase (Na+/K+ATPase), phosphatases, and several other enzyme systems. Vanadium compounds enhance the effects of insulin and have been shown to lower blood glucose in experiments in diabetic animals and humans. Both acute and chronic effects of occupational exposure to vanadium pentoxide (V2O5) and other vanadium compounds have been described. They are manifested mainly as delayed but reversible irritation of the respiratory tract involving excess mucus production and prolonged coughing, accompanied in cases of more severe exposure by bronchospasm, wheezing, and diarrhea. Eye irritation and conjunctivitis have been reported in workers. Tracheobronchitis may result from heavy, long-term exposure. Changes in lung function indicating obstructivity and increases in inflammatory biomarkers have been demonstrated in boiler cleaners after prolonged exposure. Vanadium is not mutagenic in the Ames test. However, pentavalent and tetravalent vanadium compounds have produced aneuploidy in somatic cells invitro and invivo. Clear evidence of carcinogenic activity has been shown in mice after inhalation of V2O5. The International Agency for Research on Cancer has classified V2O5as a possible carcinogen (Group 2B). Biological monitoring of vanadium in serum, blood, and urine is used to assess exposure to vanadium compounds in occupational and population studies. Reviews on environmental, toxicological and occupational health aspects of vanadium and vanadium compounds have been published (143,93,12,54,219,95,15,90,59,91,88,89and97).
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