Dietary Aflatoxin G1 exposure causes an imbalance between pulmonary tissue-resident alveolar macrophages and monocyte-derived macrophages in both mother and offspring mice.

Aflatoxin G1 (AFG1) is a mycotoxin commonly found in agricultural products, including dried fruits, meat, and milk products. Oral AFG1 administration induced tumor necrosis factor (TNF)-α-dependent chronic pulmonary inflammation, promoting AFG1-induced damage in alveolar epithelial cell, which is associated with lung adenocarcinoma. Pulmonary macrophages may be divided into tissue-resident alveolar macrophages (TRAMs) and monocyte-derived macrophages (MoMs), which involve in chronic lung inflammation. However, whether these macrophages contribute to AFG1-induced chronic pulmonary inflammation remains unknown. In this study, we found oral AFG1 administration disrupted the balance between TRAMs and MoMs, increasing MoMs infiltration and decreasing the number of TRAMs. AFG1 upregulated TNF-α expression in MoMs, but downregulated sialic acid binding Ig-like lectin F (Siglec-F) expression in TRAMs. Inhibition of TNF-α-dependent inflammation rescued the imbalance between TRAMs and MoMs in AFG1-treated lung tissues. Additionally, AFG1 stimulated MoMs differentiation to the proinflammatory M1 phenotype in vitro. Using a specific in vitro TRAM model, AFG1 downregulated Siglec-F and the M2 phenotypic markers arginase 1 and YM1, and upregulated the M1 phenotypic markers IL-6, iNOS and TNF-α, altering the TRAMs phenotype to the pro-inflammatory M1 phenotype in vitro. Additionally, mouse maternal dietary exposure to AFG1 caused an imbalance in pulmonary macrophages, decreasing TRAMs and increasing MoMs population in offspring, which was associated with proliferative lesions in the alveolar septa. Thus, dietary AFG1 exposure triggered an imbalance in pulmonary macrophages in both mother and offspring mice, and induced pro-inflammatory phenotypic alterations, which contributed to AFG1-induced chronic lung inflammation. These results provide clues to how AFG1-induced immunotoxicity and genotoxicity in humans might be prevented.

Estimation of the Dietary Acrylamide Exposure of the Turkish Population: An Emerging Threat for Human Health.

Acrylamide is a contaminant formed during heat treatment that poses potential health risks and occurs naturally in foods. Therefore, it is crucial to evaluate exposure from the consumption of foods containing acrylamide since dietary exposure continues throughout life. In this study, the acrylamide exposure level of people living in Türkiye is estimated. Consumption of a total of 28 foods in 9 different food groups was calculated using a deterministic model under two different scenarios. The exposure levels were evaluated in terms of carcinogenic, non-carcinogenic and neurotoxic health risks. The daily total acrylamide exposure levels of individuals aged 15 and older were determined as 58 µg/day (0.85 µg/kg bw/day) and 196 µg/day (2.80 µg/kg bw/day) for the good and bad scenarios, respectively. The highest daily acrylamide exposure in the good scenario came from brewed black tea (29%), whereas French fries (50%) were the source of highest daily acrylamide exposure in the bad scenario. According to the hazard index (HI) and margin of exposure (MOE) data, the good scenario (all food) is considered safe, while the bad scenario (all food) has potential and serious health risks. According to the carcinogenic risk (CR) data, both scenarios carry significant health risks. It is therefore important that consumers, producers and official institutions collaborate and take measures to reduce acrylamide exposure.

Dietary protein affects tissue accumulation of mercury and induces hepatic Phase I and Phase II enzyme expression after co-exposure with methylmercury in mice.

Methylmercury (MeHg) is a ubiquitous environmental contaminant, well known for its neurotoxic effects. MeHg can interact with several nutrients in the diet and affect nutrient metabolism, however the interaction between MeHg and dietary proteins has not been thoroughly investigated. Male BALB/c mice were fed diets based on either casein, cod or chicken as protein sources, which were or were not spiked with MeHg (3.5 mg Hg kg-1). Following 13 weeks of dietary exposure to MeHg, the animals accumulated mercury in a varying degree depending on the diet, where the levels of mercury were highest in the mice fed casein and MeHg, lower in mice fed cod and MeHg, and lowest in mice fed chicken and MeHg in all tissues assessed. Assessment of gut microbiota revealed differences in microbiota composition based on the different protein sources. However, the introduction of MeHg eliminated this difference. Proteomic profiling of liver tissue uncovered the influence of the dietary protein sources on a range of enzymes related to Phase I and Phase II detoxification mechanisms, suggesting an impact of the diet on MeHg metabolism and excretion. Also, enzymes linked to pathways including methionine and glycine betaine cycling, which in turn impact the production of glutathione, an important MeHg conjugation molecule, were up-regulated in mice fed chicken as dietary protein. Our findings indicate that dietary proteins can affect expression of hepatic enzymes that potentially influence MeHg metabolism and excretion, highlighting the relevance of considering the dietary composition in risk assessment of MeHg through dietary exposure.

Ancestral lineages of dietary exposure to an endocrine disrupting chemical drive distinct forms of transgenerational subfertility in an insect model.

Across the globe, many species of insects are facing population decline. This is largely driven by anthropogenic changes to the environment, including the widespread exposure of invertebrates to endocrine disrupting chemicals (EDCs), which impair fertility. To test whether generations of Drosophila melanogaster born from parents exposed to a common dietary EDC, equol, could recover reproductive function, we quantified the reproductive capacity of the two subsequent generations. Using a novel suite of flow cytometry assays to assess sperm functionality in real time, we find that sperm function is compromised across three generations, even after non-exposed in individuals contribute to the breeding population. Though the sex ratio alters in response to EDC exposure, favouring the survival of female offspring, most lineages with ancestral EDC exposure exhibit persistent subfertility in both the male and female. Male offspring with ancestral EDC exposure present with reduced fertility and dysfunctional spermatozoa, whereby spermatozoa are metabolically stressed, lack DNA integrity and present with permanent epigenetic alterations. Across generations, male and female offspring demonstrate distinct patterns of reproductive characteristics, depending upon the specific lineage of EDC exposure. Our results illustrate how dietary EDCs present in agricultural plants could promote transgenerational subfertility and contribute to declining insect populations.

Dietary Exposure to Pesticide and Veterinary Drug Residues and Their Effects on Human Fertility and Embryo Development: A Global Overview.

Drug residues that contaminate food and water represent a serious concern for human health. The major concerns regard the possible irrational use of these contaminants, since this might increase the amplitude of exposure. Multiple sources contribute to the overall exposure to contaminants, including agriculture, domestic use, personal, public and veterinary healthcare, increasing the possible origin of contamination. In this review, we focus on crop pesticides and veterinary drug residues because of their extensive use in modern agriculture and farming, which ensures food production and security for the ever-growing population around the world. We discuss crop pesticides and veterinary drug residues with respect to their worldwide distribution and impacts, with special attention on their harmful effects on human reproduction and embryo development, as well as their link to epigenetic alterations, leading to intergenerational and transgenerational diseases. Among the contaminants, the most commonly implicated in causing such disorders are organophosphates, glyphosate and antibiotics, with tetracyclines being the most frequently reported. This review highlights the importance of finding new management strategies for pesticides and veterinary drugs. Moreover, due to the still limited knowledge on inter- and transgenerational effects of these contaminants, we underlie the need to strengthen research in this field, so as to better clarify the specific effects of each contaminant and their long-term impact.

Influence of Genetic Polymorphisms on Cognitive Function According to Dietary Exposure to Bisphenols in a Sample of Spanish Schoolchildren.

BACKGROUND: Neurodevelopmental disorders (NDDs) like intellectual disability (ID) are highly heritable, but the environment plays an important role. For example, endocrine disrupting chemicals (EDCs), including bisphenol A (BPA) and its analogues, have been termed neuroendocrine disruptors. This study aimed to evaluate the influence of different genetic polymorphisms (SNPs) on cognitive function in Spanish schoolchildren according to dietary bisphenol exposure. METHODS: A total of 102 children aged 6-12 years old were included. Ten SNPs in genes involved in brain development, synaptic plasticity, and neurotransmission (BDNF, NTRK2, HTR2A, MTHFR, OXTR, SLC6A2, and SNAP25) were genotyped. Then, dietary exposure to bisphenols (BPA plus BPS) was estimated and cognitive functions were assessed using the WISC-V Spanish form. RESULTS: BDNF rs11030101-T and SNAP25 rs363039-A allele carriers scored better on the fluid reasoning domain, except for those inheriting the BDNF rs6265-A allele, who had lower scores. Secondly, relevant SNP-bisphenol interactions existed in verbal comprehension (NTRK2 rs10868235 (p-int = 0.043)), working memory (HTR2A rs7997012 (p-int = 0.002), MTHFR rs1801133 (p-int = 0.026), and OXTR rs53576 (p-int = 0.030)) and fluid reasoning (SLC6A2 rs998424 (p-int = 0.004)). CONCLUSIONS: Our findings provide the first proof that exploring the synergistic or additive effects between genetic variability and bisphenol exposure on cognitive function could lead to a better understanding of the multifactorial and polygenic aetiology of NDDs.

Dietary Exposure to Acrylamide Has Negative Effects on the Gastrointestinal Tract: A Review.

Changing eating habits and an increase in consumption of thermally processed products have increased the risk of the harmful impact of chemical substances in food on consumer health. A 2002 report by the Swedish National Food Administration and scientists at Stockholm University on the formation of acrylamide in food products during frying, baking and grilling contributed to an increase in scientific interest in the subject. Acrylamide is a product of Maillard's reaction, which is a non-enzymatic chemical reaction between reducing sugars and amino acids that takes place during thermal processing. The research conducted over the past 20 years has shown that consumption of acrylamide-containing products leads to disorders in human and animal organisms. The gastrointestinal tract is a complex regulatory system that determines the transport, grinding, and mixing of food, secretion of digestive juices, blood flow, growth and differentiation of tissues, and their protection. As the main route of acrylamide absorption from food, it is directly exposed to the harmful effects of acrylamide and its metabolite-glycidamide. Despite numerous studies on the effect of acrylamide on the digestive tract, no comprehensive analysis of the impact of this compound on the morphology, innervation, and secretory functions of the digestive system has been made so far. Acrylamide present in food products modifies the intestine morphology and the activity of intestinal enzymes, disrupts enteric nervous system function, affects the gut microbiome, and increases apoptosis, leading to gastrointestinal tract dysfunction. It has also been demonstrated that it interacts with other substances in food in the intestines, which increases its toxicity. This paper summarises the current knowledge of the impact of acrylamide on the gastrointestinal tract, including the enteric nervous system, and refers to strategies aimed at reducing its toxic effect.

Human exposure to per- and polyfluoroalkyl substances (PFAS) via the consumption of fish leads to exceedance of safety thresholds.

Per- and polyfluoroalkyl substances (PFAS) receive global attention due to their adverse effects on human health and the environment. Fish consumption is a major source of human PFAS exposure. The aim of this work was to address the lack of harmonization within legislations (in the EU and the USA) and highlight the level of PFAS in fish exposed to pollution from diffuse sources in the context of current safety thresholds. A non-exhaustive literature review was carried out to obtain PFAS concentrations in wild fish from the Norwegian mainland, Svalbard, the Netherlands, the USA, as well as sea regions (North Sea, English Channel, Atlantic Ocean), and farmed fish on the Dutch market. Median sum wet weight concentrations of PFOA, PFNA, PFHxS, and PFOS ranged between 0.1 µg kg-1 (farmed fish) and 22 µg kg-1 (Netherlands eel). Most concentrations fell below the EU environmental quality standard (EQSbiota) for PFOS (9.1 µg kg-1) and would not be defined as polluted in the EU. However, using recent tolerable intake or reference dose values in the EU and the USA revealed that even limited fish consumption would lead to exceedance of these thresholds - possibly posing a challenge for risk communication.

Comprehensive identification and risk assessment of regulated and emerging mycotoxins in infant foods and related raw materials and risk management advice: A case study of an infant food company in China.

This study evaluated muti-mycotoxins in 199 samples including processed infant foods and raw materials collected randomly from an infant food company and assessed their role in dietary exposure in infants and young children via probabilistic risk assessment. Approximately 79.6 % (74/93) of the processed infant foods and 65.1 % (69/106) of the raw materials were contaminated by mycotoxins, with a mean occurrence level of 3.66-321.8 µg/kg. Deoxynivalenol (DON) and tenuazonic acid (TeA) were the more prevalent mycotoxins detected, based on their higher frequencies and levels across samples. Co-occurrence of more than two mycotoxins was detected in 61.3 % (57/93) of the processed infant foods and 53.8 % (57/106) of the raw materials. Wheat flour and derived products (e.g., infant noodles and infant biscuits) were contaminated with higher contamination levels and a greater variety of mycotoxins than other samples (e.g., infant cereal and rice grains). The estimated daily exposure to OTA, DON, ZEN, and TEN was lower than the corresponding reference health-based guidance values, indicating acceptable health risks. However, the estimated dietary exposure to alternariol monomethyl ether (AME), alternariol (AOH), and tenuazonic acid (TeA) exceeded the corresponding thresholds of toxicological concern values, indicating potential dietary intake risks. Among the various samples, cereals and cereal-based infant foods emerged as the primary contributors to mycotoxin exposure. Further research is advised to address the uncertainties surrounding the toxicity associated with emerging Alternaria mycotoxins and to conduct cumulative risk assessments concerning multiple mycotoxin exposure in infants and young children.

Infant exposure to ochratoxin A, zearalenone, and deoxynivalenol from the consumption of milk formula and baby cereal in Chile.

Ochratoxin A (OTA), zearalenone (ZEN), and deoxynivalenol (DON) are mycotoxins whose exposure is associated with various adverse health effects, including cancer and renal disorders, estrogenic effects, and immunosuppressive and gastrointestinal disorders, respectively. Infants (<2 years) are the most vulnerable group to mycotoxins, representing a unique combination of restricted food consumption types, low body weight, lower ability to eliminate toxins, and more future years to accumulate toxins. This study aimed to estimate the infant́s exposure to OTA, DON, and ZEN due to the consumption of milk formula and baby cereals in Chile. Milk formula samples (n = 41) and baby cereals (n = 30) were collected and analyzed using commercial ELISA kits for OTA, DON, and ZEA determination. Exposure was assessed by the Estimated Daily Intake (EDI) approach (mean and worst-case scenario, WCS) with the levels found in a modified Lower Bound (mLB) and Upper Bound (UB); ideal consumption (<6m, 7-12 m, and 13-24 m); adjusted by the weight of each group. The risk was estimated by comparing the EDI with a reference tolerable daily intake or by the margin of exposure (MOE) in the case of OTA. DON and OTA occurrence in infant formula were 34 % and 41 %, respectively. The co-occurrence between these mycotoxins was 22 %. Mycotoxin contents were below LOQ values except for OTA determined in one sample (0.29 ng/ml). No milk formulae were contaminated with ZEN. In the case of baby cereals, the occurrences were 17 % for OTA, 30 % for DON, and 7 % for ZEN, all below LOQ. Co-occurrence was seen in two samples between ZEN and OTA. According to exposure calculations, the MOE for OTA was less than 10,000 in all models for milk formula between 0 to 12 months of age and in the UB and WCS for cereal consumption. Health concerns were observed for DON in the WCS and UB for milk consumption in all ages and only in the UB WCS for cereal consumption. Considering the high consumption of milk formula in these age groups, regulation of OTA and other co-occurring mycotoxins in infant milk and food is strongly suggested.

Commentary of the SKLM to the EFSA opinion on risk assessment of N-nitrosamines in food.

Dietary exposure to N-nitrosamines has recently been assessed by the European Food Safety Authority (EFSA) to result in margins of exposure that are conceived to indicate concern with respect to human health risk. However, evidence from more than half a century of international research shows that N-nitroso compounds (NOC) can also be formed endogenously. In this commentary of the Senate Commission on Food Safety (SKLM) of the German Research Foundation (DFG), the complex metabolic and physiological biokinetics network of nitrate, nitrite and reactive nitrogen species is discussed with emphasis on its influence on endogenous NOC formation. Pioneering approaches to monitor endogenous NOC have been based on steady-state levels of N-nitrosodimethylamine (NDMA) in human blood and on DNA adduct levels in blood cells. Further NOC have not been considered yet to a comparable extent, although their generation from endogenous or exogenous precursors is to be expected. The evidence available to date indicates that endogenous NDMA exposure could exceed dietary exposure by about 2-3 orders of magnitude. These findings require consolidation by refined toxicokinetics and DNA adduct monitoring data to achieve a credible and comprehensive human health risk assessment.

Occurrence of mycotoxins in meat alternatives: Dietary exposure, potential health risks, and burden of disease.

This study aimed to present the occurrence of sixteen mycotoxins in 105 meat alternatives based on wheat, legumes, and vegetables from Italy. The targeted mycotoxins were aflatoxins (AFB1, AFB2, AFG1, AFG2), fumonisins B1 and B2 (FB1, FB2), alternariol (AOH), alternariol monomethyl ether (AME), tentoxin (TEN), ochratoxin A (OTA), zearalenone (ZEN), T-2/HT-2 toxin, deoxynivalenol (DON), enniatin B (ENNB), and beauvericin (BEA). The occurrence of mycotoxins was between 0% (AFB2) - 97.4% (ENNB). Mycotoxin co-occurrence varied from binary combinations up to mixtures of twelve. To assess the dietary exposure and potential health risks we simulated the replacement of meat consumption for Italian consumers with meat alternatives. The cumulative exposure to Alternaria mycotoxins and trichothecenes indicated a potential health risk while the exposure to aflatoxins and ochratoxin A indicated a potential health concern related to liver and renal cancer in the model scenario. Moreover, we estimated the risk of liver cancer from exposure to AFB1 and quantified the potential burden using Disability-Adjusted Life Years (DALYs). Luckily, the potential risk of liver cancer was low between 0 and 0.05/100,000 individuals with an associated burden of disease of 0.83 DALYs/100,000 individuals. Taking into consideration the presence of meat alternatives on the food market and the ongoing shift towards plant-based diets there is a need for continuous monitoring to keep the occurrence at safe levels. More attention is needed from the regulatory side for policymakers to consider the legislations of mycotoxins in meat alternatives.

Toxicological assessment of dietary exposure of polyethylene microplastics on growth, nutrient digestibility, carcass and gut histology of Nile Tilapia (Oreochromis niloticus) fingerlings.

This study was conducted to ascertain the negative effects of dietary low-density polyethylene microplastics (LDPE-MPs) exposure on growth, nutrient digestibility, body composition and gut histology of Nile tilapia (Oreochromis niloticus). Six sunflower meal-based diets (protein 30.95%; fat 8.04%) were prepared; one was the control (0%) and five were incorporated with LDPE-MPs at levels of 2, 4, 6, 8 and 10% in sunflower meal-based diets. A total of eighteen experimental tanks, each with 15 fingerlings, were used in triplicates. Fish were fed at the rate of 5% biomass twice a day for 60 days. Results revealed that best values of growth, nutrient digestibility, body composition and gut histology were observed by control diet, while 10% exposure to LDPE-MPs significantly (P < 0.05) reduced weight gain (WG%, 85.04%), specific growth rate (SGR%, 0.68%), and increased FCR (3.92%). The findings showed that higher level of LDPE-MPs (10%) exposure in the diet of O. niloticus negatively affects nutrient digestibility. Furthermore, the results revealed that the higher concentration of LDPE-MPs (10%) had a detrimental impact on crude protein (11.92%) and crude fat (8.04%). A high number of histological lesions were seen in gut of fingerlings exposed to LDPE-MPs. Hence, LDPE-MPs potentially harm the aquatic health.

Biochemical, molecular, and physiological assessments of crude oil dietary exposure in sub-adult red drum (Sciaenops ocellatus).

A 14-day exposure study in which sub-adult red drum (Sciaenops ocellatus) were fed a petroleum crude oil-treated pellet feed was conducted to assess the potential effects of ingesting an oil-contaminated food source. Though food consumption decreased, significant polycyclic aromatic hydrocarbons accumulated in the body and liver, which did not affect the body and liver's fatty acid composition. In the red drum given the crude oil-treated feed, a significant decrease in the RNA:DNA growth rate index was noted, while only subtle changes in body and liver lipid composition were seen. Differentially expressed gene analysis in the liver demonstrated a significant down-regulation of leptin and up-regulation of the aryl hydrocarbon receptor nuclear translocator-like protein 1. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses indicated enrichment of terms and pathways associated with cholesterol biosynthesis and oxidative stress. Ingenuity Pathway Analysis further predicted activation of seven pathways associated with cholesterol biosynthesis. Measured oxidative stress biomarkers in the blood indicated decreased systemic antioxidants with increased lipid peroxidation. The results of this study suggest that dietary oil exposure alters the signaling of biological pathways critical in cholesterol biosynthesis and disruptions in systemic oxidative homeostasis.

Dietary aflatoxins exposure, environmental enteropathy, and their relation with childhood stunting.

Childhood stunting is a global phenomenon affecting more than 149 million children under the age of 5 worldwide. Exposure to aflatoxins (AFs) in utero, during breastfeeding, and consumption of contaminated food affect the gut microbiome, resulting in intestinal dysfunction and potentially contributing to stunting. This review explores the potential relationship between AF exposure, environmental enteropathy and childhood stunting. AFs bind to DNA, disrupt protein synthesis and elicit environmental enteropathy (EE). An EE alters the structure of intestinal epithelial cells, impairs nutrient uptake and leads to malabsorption. This article proposes possible intervention strategies for researchers and policymakers to reduce AF exposure, EE and childhood stunting, such as exposure reduction, the implementation of good agricultural practices, dietary diversification and improving environmental water sanitation and hygiene.

Dietary Emulsifier Exposure in People With Inflammatory Bowel Disease Compared With Healthy Controls: Is There a Cause for Concern?

BACKGROUND: Emulsifiers are implicated in the pathogenesis of inflammatory bowel disease (IBD). Few studies have examined emulsifier intake in people with existing IBD. We aimed to describe the frequency of exposure to 6 selected emulsifiers in a contemporary cohort of people with IBD and compare intake with healthy controls (HCs). METHODS: Baseline food records from participants in an Australian prospective cohort study examining the microbiome of IBD patients and HCs were analyzed. Exposure to inflammatory emulsifiers polysorbate-80 (P80); carboxymethylcellulose (CMC); carrageenan; xanthan gum (XG); lecithin (soy and sunflower) and mono- and diglycerides of fatty acids (MDGs) were determined by examining ingredient lists. Frequency of emulsifier exposure between groups (IBD vs HC, Crohn's disease [CD] vs ulcerative colitis [UC], IBD children vs adults, active disease vs remission) was examined after controlling for confounders. RESULTS: Records from 367 participants were analyzed (n = 176 IBD, of which there were 101 CD, 75 UC, and 191 HC patients). In total, 5022 unique food items were examined, with 18% containing 1 or more emulsifier of interest. Inflammatory bowel disease participants had significantly higher total daily emulsifier exposure compared with HCs (2.7 ±â€…1.8 vs 2.3 ±â€…1.6, P = .02). In IBD participants, emulsifiers with the highest daily exposure were MDGs (1.2 ±â€…0.93), lecithin (0.85 ±â€…0.93), and XG (0.38 ±â€…0.42). There were no recorded exposures to P80. CONCLUSIONS: Inflammatory bowel disease participants were exposed to more emulsifiers than HCs. Intake of inflammatory emulsifiers were low or nonexistent, suggesting their presence in the food supply are not as common as frequently stated.

Prenatal dietary exposure to mixtures of chemicals is associated with allergy or respiratory diseases in children in the ELFE nationwide cohort.

INTRODUCTION: Prenatal exposure to environmental chemicals may be associated with allergies later in life. We aimed to examine the association between prenatal dietary exposure to mixtures of chemicals and allergic or respiratory diseases up to age 5.5 y. METHODS: We included 11,638 mother-child pairs from the French "Étude Longitudinale Française depuis l'Enfance" (ELFE) cohort. Maternal dietary exposure during pregnancy to eight mixtures of chemicals was previously assessed. Allergic and respiratory diseases (eczema, food allergy, wheezing and asthma) were reported by parents between birth and age 5.5 years. Associations were evaluated with adjusted logistic regressions. Results are expressed as odds ratio (OR[95%CI]) for a variation of one SD increase in mixture pattern. RESULTS: Maternal dietary exposure to a mixture composed mainly of trace elements, furans and polycyclic aromatic hydrocarbons (PAHs) was positively associated with the risk of eczema (1.10 [1.05; 1.15]), this association was consistent across sensitivity analyses. Dietary exposure to one mixture of pesticides was positively associated with the risk of food allergy (1.10 [1.02; 1.18]), whereas the exposure to another mixture of pesticides was positively but slightly related to the risk of wheezing (1.05 [1.01; 1.08]). This last association was not found in all sensitivity analyses. Dietary exposure to a mixture composed by perfluoroalkyl acids, PAHs and trace elements was negatively associated with the risk of asthma (0.89 [0.80; 0.99]), this association was consistent across sensitivity analyses, except the complete-case analysis. CONCLUSION: Whereas few individual chemicals were related to the risk of allergic and respiratory diseases, some consistent associations were found between prenatal dietary exposure to some mixtures of chemicals and the risk of allergic or respiratory diseases. The positive association between trace elements, furans and PAHs and the risk of eczema, and that between pesticides mixtures and food allergy need to be confirmed in other studies. Conversely, the negative association between perfluoroalkyl acids, PAHs and trace elements and the risk of asthma need to be further explored.

Associations between dietary pesticide residue mixture exposure and mortality in a population-based prospective cohort of men and women.

BACKGROUND: There is a concern that pesticide residues, regularly detected in foods, might pose a health risk to the consumer, but epidemiological evidence is limited. We assessed the associations between dietary exposure to a mixture of pesticide residues and mortality. METHODS: Food consumption was assessed in 68,844 participants from the Swedish Mammography Cohort and the Cohort of Swedish Men, 45-83 years at baseline (1997). Concentrations of pesticide residues detected in foods on the Swedish market (1996-1998), mainly fruits and vegetables, were obtained via monitoring programs. To assess mixture effects, we summed per food item the ratios of each single pesticide mean residue concentration divided by its acceptable daily intake to create for each participant a Dietary Pesticide Hazard Index (adjusted for energy intake and expressed per kilogram of body weight). Multivariable-adjusted Cox proportional hazards models were used to estimate hazard ratios (HR) and 95 % confidence intervals (95 %CI). RESULTS: During 15 years of follow-up (1998-2014), a total of 16,527 deaths occurred, of which 6,238 were caused by cardiovascular disease (CVD) and 5,364 by cancer. Comparing extreme quintiles of Dietary Pesticide Hazard Index, the highest category was inversely associated with CVD mortality HR, 0.82 (95 % CI, 0.75-0.90) and with cancer mortality HR 0.82 (95 % CI 0.75-0.91). In analyses stratified by high/low Dietary Pesticide Hazard Index, similar inverse associations were observed by increasing fruit and vegetable consumption. CONCLUSIONS: We observed no indications that dietary exposure to pesticide residue mixtures was associated with increased mortality, nor any clear indications that the benefits of fruit and vegetable consumption on mortality was compromised. Yet, our results need to be interpreted with caution.

[Probabilistic risk assessment of dietary exposure to lead among Chongqing residents].

OBJECTIVE: To investigate lead contamination in commercial foods in Chongqing City, and to assess the health risk of dietary lead exposure of residents in Chongqing City. METHODS: Lead concentration data was obtained from the food safety risk monitoring system, which included a total of 2347 lead-containing food samples in 11 categories in Chongqing from 2016 to 2020. Consumption data was derived from the China Health and Nutrition Survey Project in Chongqing in 2018(3 day, 24 h dietary recall survey). The dietary exposure to lead of residents in Chongqing was calculated by the Monte Carlo simulation method and the margin of exposure(MOE) method was used to evaluate the health risk of the population. RESULTS: The average content of lead in 2347 food samples from 11 categories ranged from 0.0328 to 0.0363 mg/kg, with an overall detection rate of 58.5%. For people aged between 3-6, 7-17, 18-59, and ≥ 60 years, the mean dietary lead intakes in Chongqing were 0.935-1.070, 0.600-0.684, 0.367-0.416, 0.369-0.419 µg/(kg·BW·d), respectively; and the high levels of dietary lead exposure(P95) were 1.642-1.852, 1.147-1.299, 0.651-0.729, 0.659-0.740 µg/(kg·BW·d), respectively. MOE values for lead were less than 1 for age groups 3-6 and 7-17 years. Mean MOE values for lead were greater than 1 for ages 18 to 59 and ≥ 60. Cereals and their products, vegetables and their products, and meat and meat products were the main sources of dietary lead exposure, accounting for more than 85% of the total dietary lead exposure. CONCLUSION: There are potential health risks of lead for residents in Chongqing.

Chronic Health Risk for Chinese Adults and Breastfed Infants on Dietary Exposure to Chlorothalonil and Its Main Metabolite.

This study presents the first nationwide study on the chronic health risks of chlorothalonil and its metabolite (4-OH-chlorothalonil) for Chinese adults and breastfed infants via dietary intake. The determination of chlorothalonil and 4-OH-chlorothalonil in dietary samples was accomplished by cold-induced liquid-liquid extraction using liquid chromatography─high-resolution mass spectrometry. Chlorothalonil and 4-OH-chlorothalonil were detected in 43.1 and 46.1% of total dietary samples, respectively, while only 4-OH-chlorothalonil was detected in 100% of breast milk samples. Chlorothalonil and 4-OH-chlorothalonil residues in dietary samples of Northwest China and Shandong regions were higher in comparison to those of other regions. No correlation between 4-OH-chlorothalonil residues in breast milk and adult daily dietary intake to total chlorothalonil indicates the presence of other exposure routes besides dietary exposure. Furthermore, a residue analysis of 4-OH-chlorothalonil in breast milk between urban and rural areas in all sampling locales showed no statistical difference (p > 0.05). The findings of this study reveal that the chronic health risks caused by dietary exposure to chlorothalonil and 4-OH-chlorothalonil are low for Chinese adults and breastfed infants.