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Background: The EAT-Lancet diet was created to support dietary transition towards sustainable diets. Current evidence indicates that adherence to the EAT-Lancet diet may reduce mortality risk, yet how adherence may impact dietary exposure to food contaminants remains unexplored. We aimed to estimate the association between adherence to the EAT-Lancet diet and i) all-cause, cardiovascular-, and cancer-mortality and ii) predicted dietary exposure to the following food contaminants: cadmium, methylmercury, polychlorinated biphenyls (PCBs), and pesticide residues., Methods: We used self-reported dietary data from a 96-item food frequency questionnaire of two population-based cohorts - the Cohort of Swedish Men (n = 35,687) and the Swedish Mammography Cohort (n = 32,488). The EAT-Lancet Adherence Index (EAI) was created by scoring consumption of the 14 dietary components included in the EAT-Lancet diet (totalling 0-14 points). Cox proportional hazards regression models were applied to assess the association between EAI and mortality outcomes, presented as multivariable-adjusted hazard ratios (HR) and 95 % confidence intervals (CI). Descriptive statistics were used to characterise predicted exposure to food contaminants, and the correlations between EAI and food contaminants assessed using Spearman's rank correlation., Results: Increased adherence to the EAT-Lancet diet was associated with a lower risk of all-cause mortality (per 3-point increase in EAI: HR = 0.93; CI:0.90,0.97 and HR = 0.91; CI:0.87,0.95 for men and women, respectively) and cardiovascular-mortality (corresponding HR = 0.94; CI:0.88,1.00 and HR = 0.93; CI:0.87,1.00). No clear association was found with cancer-mortality. Increasing EAI was correlated with increased predicted dietary exposure to cadmium, methylmercury, PCBs, and pesticide residues and their median predicted dietary exposures were greater in the high adherence group, compared to the low adherence group., Conclusion: High adherence to the EAT-Lancet diet is associated with a reduction in risk of all-cause and cardiovascular-mortality, but also increased dietary exposure to food contaminants., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Beneficial effects of fish consumption on heart failure (HF) may be modified by contaminants in fish. Polychlorinated biphenyls (PCBs) are of particular concern as they have been associated with well-established risk factors of HF, but current data are limited., Objectives: We aimed to assess the association between dietary PCB exposure and risk of HF, accounting for dietary intake of long-chain omega-3 fish fatty acids., Design: We used the prospective population-based research structure SIMPLER (previously the Swedish Mammography Cohort and Cohort of Swedish Men) comprising 32,952 women and 36,546 men, free from cancer, cardiovascular disease and diabetes at baseline in 1997. Validated estimates of dietary PCBs and long-chain omega-3 fish fatty acids [eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA)] were obtained via a food frequency questionnaire at baseline. Incident cases of HF were ascertained through register linkage., Results: During an average of 12 years of follow-up, we ascertained 2736 and 3128 incident cases of HF in women and men, respectively. In multivariable-adjusted models, mutually adjusted for PCBs and EPA-DHA, the relative risk (RR) for dietary PCB exposure was 1.48 (95% CI 1.12-1.96) in women and 1.42 (95% CI 1.08-1.86) in men, comparing extreme quintiles. Corresponding RRs for EPA-DHA intake were 0.71 (95% CI 0.54-0.93) and 0.82 (95% CI 0.63-1.07), respectively., Conclusions: Dietary exposure to PCBs was associated with an increased risk of HF in both women and men. EPA-DHA intake was associated with a lower risk of HF in women, with a similar tendency in men., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: For malignant melanoma, other risk factors aside from sun exposure have been hardly explored. Polychlorinated biphenyls (PCBs)-mainly from fatty fish- may affect melanogenesis and promote melanoma progression, while long-chain n-3 polyunsaturated fatty acids seem to exert antineoplastic actions in melanoma cells., Objectives: We aimed to assess the association of validated estimates of dietary PCB exposure as well as the intake of eicosapentaenoic acid and docosahexaenoic acid (EPA-DHA), accounting for sun habits and skin type, with the risk of malignant melanoma in middle-aged and elderly women., Methods: We included 20,785 women at baseline in 2009 from the prospective population-based Swedish Mammography Cohort. Validated estimates of dietary PCB exposure and EPA-DHA intake were obtained via a food frequency questionnaire. Incident melanoma cases were ascertained through register-linkage., Results: During 4.5 years of follow-up, we ascertained 67 incident cases of melanoma. After multivariable adjustments, exposure to dietary PCBs was associated with four-fold increased risk of malignant melanoma (hazard ratio [HR], 4.0 [95% confidence interval {CI}, 1.2-13; P for trend = 0.02]), while EPA-DHA intake was associated with 80% lower risk (HR, 0.2 [95% CI, 0.1-0.8; P for trend = 0.03]), comparing the highest exposure tertiles with the lowest., Conclusion: While we found a direct association between dietary PCB exposure and risk of melanoma, EPA-DHA intake showed to have a substantial protective association. Question of benefits and risk from fish consumption is very relevant and further prospective studies in the general population verifying these findings are warranted., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Polychlorinated biphenyls (PCBs) are highly persistent environmental pollutants and are undesirable components of our daily food. PCBs are classified as human carcinogens, but the evidence for prostate cancer is limited and available data are inconsistent. We explored the link between non-dioxin-like PCB and grade of prostate cancer in a prospective cohort as well as in cell experiments. A population-based cohort of 32496 Swedish men aged 45-79 years was followed prospectively through 1998-2011, to assess the association between validated estimates of dietary PCB exposure and incidence of prostate cancer by grade (2789 cases, whereof 1276 low grade, 756 intermediate grade, 450 high grade) and prostate cancer mortality (357 fatal cases). In addition, we investigated a non-dioxin-like PCB153-induced cell invasion and related markers in normal prostate stem cells (WPE-stem) and in three different prostate cancer cell lines (PC3, DU145 and 22RV1) at exposure levels relevant to humans. After multivariable-adjustment, dietary PCB exposure was positively associated with high-grade prostate cancer, relative risk (RR) 1.35 [95% confidence interval (CI): 1.03-1.76] and with fatal prostate cancer, RR 1.43 (95% CI: 1.05-1.95), comparing the highest tertile with the lowest. We observed no association with low or intermediate grade of prostate cancer. Cell invasion and related markers, including MMP9, MMP2, Slug and Snail, were significantly increased in human prostate cancer cells as well as in prostate stem cells after exposure to PCB153. Our findings both from the observational and experimental studies suggest a role of non-dioxin-like PCB153 in the development of high-grade and fatal prostate cancer., (© The Author 2016. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Background: Observational studies on polychlorinated biphenyl (PCB) exposure and hormone-related cancer risk are either inconsistent or lacking. We aimed to assess associations of dietary PCB exposure with breast, endometrial and ovarian cancer risk in middle-aged and elderly women., Methods: We included 36 777 cancer-free women at baseline in 1997 from the prospective population-based Swedish Mammography Cohort. Validated estimates of dietary PCB exposure were obtained via a food frequency questionnaire. Incident cancer cases were ascertained through register linkage., Results: During 14 years of follow-up, we ascertained 1593, 437 and 195 incident cases of breast, endometrial and ovarian cancer. We found no overall association between dietary PCB exposure and any of these cancer forms. The multivariable-adjusted relative risks comparing women in the highest and lowest tertile of PCB exposure were 0.96 (95% confidence interval (CI): 0.75, 1.24), 1.21 (95% CI: 0.73, 2.01) and 0.90 (95% CI: 0.45, 1.79) for breast, endometrial and ovarian cancer. In analyses stratified by factors influencing oestrogen exposure, possibly masking associations with PCBs, indications of higher risks were observed for endometrial cancer., Conclusions: This study suggests that dietary exposure to PCBs play no critical role in the development of breast, endometrial or ovarian cancer during middle-age and old ages.

Background: Little is known about joint exposure to polychlorinated biphenyls (PCBs) and long-chain omega-3 fatty acids [eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA)], through fish consumption, on cerebrovascular disease risk., Objective: To explore associations of dietary PCB exposure and EPA-DHA intake with risk of different stroke subtypes., Methods: This was assessed in the prospective population-based Cohort of Swedish Men including 39,948, middle-aged and elderly men, who were free of cardiovascular disease and cancer at baseline in 1997. Validated estimates of dietary PCBs and EPA-DHA were obtained via a food frequency questionnaire., Results: During 12years of follow-up, 2286 and 474 incident cases of ischemic stroke and hemorrhagic stroke, respectively, were ascertained through register linkage. Dietary PCB exposure and EPA-DHA intake were associated with hemorrhagic stroke but not ischemic stroke. Men in the highest quartile of dietary PCB exposure (median 412ng/day) had a multivariable- and EPA-DHA-adjusted RR of hemorrhagic stroke of 2.77 [95% confidence interval (CI), 1.48-5.19] compared with men in the lowest quartile (median 128ng/day; p for trend <0.01). The corresponding RRs in men with and without hypertension were 5.45 (95% CI, 1.34-22.1) and 2.37 (95% CI 1.17-4.79), respectively. The multivariable- and PCB-adjusted RR of hemorrhagic stroke for the highest quartile of EPA-DHA intake (median 0.73g/day) versus the lowest quartile (median 0.18g/day) was 0.42 (95% CI, 0.22-0.79)., Conclusion: Dietary PCB exposure was associated with an increased risk of hemorrhagic stroke, whereas a protective association was observed for dietary EPA-DHA intake., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Background: Major food contaminants such as polychlorinated biphenyls (PCBs) are proposed to play a role in the etiology of cardiovascular disease (CVD), but to date the impact of PCBs on cardiovascular health need to be explored., Methods and Results: We assessed the association between validated food frequency questionnaire-based estimates of dietary PCB exposure and risk of myocardial infarction, ascertained through register-linkage, among 36,759 men from the population-based Swedish Cohort of Men, free of cardiovascular disease, diabetes and cancer at baseline (1997). Relative risks were adjusted for known cardiovascular risk factors, long-chain omega-3 fatty acids (eicosapentaenoic and docosahexaenoic acids) and methyl mercury exposure. During 12years of follow-up (433,243 person-years), we ascertained 3005 incident cases of myocardial infarction (654 fatal). Compared with the lowest quintile of dietary PCB exposure (median 113ng/day), men in the highest quintile (median 436ng/day) had multivariable-adjusted relative risks of 1.74 (95% confidence interval [CI], 1.30-2.33; p-trend<0.001) for total and 1.97 (95% CI 1.42-2.75; p-trend<0.001) for non-fatal myocardial infarction. In mutually adjusted models, dietary PCB exposure was associated with an increased risk of myocardial infarction, while the intake of long-chain omega-3 fish fatty acids was associated with a decreased risk. We also observed an effect modification by adiposity on the association between of dietary PCB exposure and myocardial infarction, with higher risk among lean men (p value for interaction =0.03)., Conclusions: Exposure to PCBs via diet was associated with increased risk of myocardial infarction in men., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Background: Fish consumption may promote cardiovascular health. The role of major food contaminants, such as polychlorinated biphenyls (PCBs) common in fatty fish, is unclear. We assessed the association between dietary PCB exposure and risk of myocardial infarction taking into account the intake of long-chain omega-3 fish fatty acids., Methods: In the prospective population-based Swedish Mammography Cohort, 33,446 middle-aged and elderly women, free from cardiovascular disease, cancer and diabetes at baseline (1997) were followed-up for 12 years. Validated estimates of dietary PCB exposure and intake of fish fatty acids (eicosapentaenoic acid and docosahexaenoic acid; EPA-DHA) were obtained via a food frequency questionnaire at baseline., Results: During follow-up 1386 incident cases of myocardial infarction were ascertained through register-linkage. Women in the highest quartile of dietary PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of myocardial infarction of 1.21 (95% confidence interval [CI], 1.01-1.45) compared to the lowest quartile (median 101 ng/day) before, and 1.58 (95% CI, 1.10-2.25) after adjusting for EPA-DHA. Stratification by low and high EPA-DHA intake, resulted in RRs 2.20 (95% CI, 1.18-4.12) and 1.73 (95% CI, 0.81-3.69), respectively comparing highest PCB tertile with lowest. The intake of dietary EPA-DHA was inversely associated with risk of myocardial infarction after but not before adjusting for dietary PCB., Conclusion: Exposure to PCBs was associated with increased risk of myocardial infarction, while some beneficial effect was associated with increasing EPA and DHA intake. To increase the net benefits of fish consumption, PCB contamination should be reduced to a minimum., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Early puberty has been found to be associated with adverse health outcomes such as metabolic and cardiovascular diseases and hormone-dependent cancers. The decrease in age at menarche observed during the past decades has been linked to an increased exposure to endocrine-disrupting compounds (EDCs). Evidence for the association between PFAS and phthalate exposure and menarche onset, however, is inconsistent. We studied the association between PFAS and phthalate/DINCH exposure and age at menarche using data of 514 teenagers (12 to 18 years) from four aligned studies of the Human Biomonitoring for Europe initiative (HBM4EU): Riksmaten Adolescents 2016–2017 (Sweden), PCB cohort (follow-up; Slovakia), GerES V-sub (Germany), and FLEHS IV (Belgium). PFAS concentrations were measured in blood, and phthalate/DINCH concentrations in urine. We assessed the role of each individual pollutant within the context of the others, by using different multi-pollutant approaches, adjusting for age, age- and sex-standardized body mass index z-score and household educational level. Exposure to di(2-ethylhexyl) phthalate (DEHP), especially mono(2-ethyl-5-hydroxyhexyl) phthalate (5OH-MEHP), was associated with an earlier age at menarche, with estimates per interquartile fold change in 5OH-MEHP ranging from −0.34 to −0.12 years in the different models. Findings from this study indicated associations between age at menarche and some specific EDCs at concentrations detected in the general European population, but due to the study design (menarche onset preceded the chemical measurements), caution is needed in the interpretation of causality. [ABSTRACT FROM AUTHOR]

Purpose: Epidemiological evidence on the association between fish consumption and risk of type 2 diabetes is heterogeneous across geographical regions. Differences related to fish consumption pattern could possibly help explain the discrepancy between the findings. We therefore aimed to investigate the association between fish consumption (total, fried, specific fish items) and type 2 diabetes incidence, taking exposure to contaminants present in fish (polychlorinated biphenyls and methyl mercury) into consideration. Methods: The population-based Cohort of Swedish Men, including 35,583 men aged 45-79 years, was followed from 1998 to 2012. We estimated hazard ratios (HRs) with 95 % confidence intervals (CIs) using Cox proportional hazards models. Results: During 15 years of follow-up, 3624 incident cases were identified. Total fish consumption (≥4 servings/week vs. <1 serving/week) was not associated with type 2 diabetes in multivariable-adjusted analysis (HR 1.00; 95 % CI 0.85-1.18); however, a statistically non-significant inverse association was observed after adjustment for dietary contaminant exposures (HR 0.79; 95 % CI 0.60-1.04). Fried fish (≥6 servings/month vs. ≤1 servings/month) and shellfish consumption (≥1 serving/week vs. never/seldom) were associated with HRs of 1.14 (95 % CI 1.03-1.31) and 1.21 (95 % CI 1.07-1.36), respectively. Conclusions: We observed no overall association between total fish consumption and type 2 diabetes. The results indicated that dietary contaminants in fish may influence the relationship. Fried fish and shellfish consumption were associated with higher type 2 diabetes incidence. These findings suggest that more specific advice on fish species sub-types (varying in contamination) and preparation methods may be warranted. [ABSTRACT FROM AUTHOR]

Arctic inhabitants are highly exposed to persistent organic pollutants (POP), which may produce adverse health effects. This study characterized alterations in tissue retinoid (vitamin A) levels in rat offspring and their dams following in utero and lactational exposure to the Northern Contaminant Mixture (NCM), a mixture of 27 contaminants including polychlorinated biphenyls (PCB), organochlorine (OC) pesticides, and methylmercury (MeHg), present in maternal blood of the Canadian Arctic Inuit population. Further, effect levels for retinoid system alterations and other endpoints were compared to the Arctic Inuit population exposure and their interrelationships were assessed. Sprague-Dawley rat dams were dosed with NCM from gestational day 1 to postnatal day (PND) 23. Livers, kidneys and serum were obtained from offspring on PND35, PND77, and PND350 and their dams on PND30 for analysis of tissue retinoid levels, hepatic cytochrome P-450 (CYP) enzymes, and serum thyroid hormones. Benchmark doses were established for all endpoints, and a partial least-squares regression analysis was performed for NCM treatment, hepatic retinoid levels, CYP enzyme induction, and thyroid hormone levels, as well as body and liver weights. Hepatic retinoid levels were sensitive endpoints, with the most pronounced effects at PND35 though still apparent at PND350. The effects on tissue retinoid levels and changes in CYP enzyme activities, body and liver weights, and thyroid hormone levels were associated and likely driven by dioxin-like compounds in the mixture. Low margins of exposure were observed for all retinoid endpoints at PND35. These findings are important for health risk assessment of Canadian Arctic populations and further support the use of retinoid system analyses in testing of endocrine-system-modulating compounds. [ABSTRACT FROM PUBLISHER]

Arctic inhabitants consume large proportions of fish and marine mammals, and are therefore continuously exposed to levels of environmental toxicants, which may produce adverse health effects. Fetuses and newborns are the most vulnerable groups. The aim of this study was to evaluate changes in bone geometry, mineral density, and biomechanical properties during development following perinatal exposure to a mixture of environmental contaminants corresponding to maternal blood levels in Canadian Arctic human populations. Sprague-Dawley rat dams were dosed with a Northern Contaminant Mixture (NCM) from gestational day 1 to postnatal day (PND) 23. NCM contains 27 contaminants comprising polychlorinated biphenyls, organochlorine pesticides, and methylmercury. Femurs were collected on PND 35, 77 and 350, and diaphysis was analyzed by peripheral quantitative computed tomography and three-point bending test, while femoral neck was assessed in an axial loading experiment. Dose-response modeling was performed to establish the benchmark dose (BMD) for the analyzed bone parameters. Exposure to the high dose of NMC resulted in short and thin femur with reduced mechanical strength in offspring at PND35. BMD of femur length, cortical area, and stiffness were 3.2, 1.6, and 0.8 mg/kg bw/d, respectively. At PND77 femur was still thin, but at PND350 no treatment-related bone differences were detected. This study provides new insights on environmental contaminants present in the maternal blood of Canadian Arctic populations, showing that perinatal exposure induces bone alterations in the young offspring. These findings could be significant from a health risk assessment point of view. [ABSTRACT FROM AUTHOR]

Abstract: Exposure to polychlorinated biphenyls (PCBs) induce a broad spectrum of toxic effects in various organs including bone. The most susceptible age-groups to the toxic effects of PCBs are foetuses and infants. The aim of the present study was to quantitatively evaluate changes in bone geometry, mineral density and biomechanical properties following perinatal exposure to the PCB mixture, Aroclor 1254 (A1254), and to examine the persistence of observed bone alterations by following the offspring over time. Sprague–Dawley rat offspring were exposed to A1254 from gestational day 1 to post-natal day (PND) 23. Femur and tibia were collected on PNDs 35, 77 and 350 and were analyzed by peripheral quantitative computed tomography and biomechanical testing. At PND35, exposure to A1254 induced short, thin femur and tibia, with reduced mechanical strength of femoral neck. No treatment-related bone changes were detected in offspring at PND77 or PND350. In conclusion, the present investigation suggests that perinatal exposure to A1254 leads to shorter, thinner and weaker bones in juvenile rats at PND35, with these effects being absent at later time-points as exposure is discontinued. The results indicate that the observed bone effects are mainly driven by the dioxin-like congeners, although it cannot exclude the contribution of the non dioxin-like congeners to the exposure outcome. [Copyright &y& Elsevier]