PMID: 

Int J Environ Res Public Health. 2019 Oct 17 ;16(20). Epub 2019 Oct 17. PMID: 31627286

Abstract Title: 

Environmental Exposure to Pesticides and Breast Cancer in a Region of Intensive Agribusiness Activity in Brazil: A Case-Control Study.

Abstract: 

: Breast cancer is a serious public health problem and is the second most prevalent cancer type in the world. The purpose of this article is to evaluate the association between pesticide use and breast cancer in a region of intense agribusiness activity in the state of Mato Grosso, Brazil.: A case-control study was conducted on women living in the city of Rondonópolis, in the south of Mato Grosso state. There were 85 cases of women with confirmed breast cancer and 266 controls who were randomly selected from primary health care users. Bivariate and stratified analyses were performed. Multiple logistic regression was then performed, keeping in the final model the factors with a significance level lower than or equal to 0.05 or considered important according to apriori biological criteria.: In the final model, living near cropland with pesticides (OR: 2.37; CI: 95% 1.78-3.16) and women aged over 50 years who experienced early menarche (OR: 2.08; CI: 95% 1.06-4.12) had a higher risk of developing breast cancer compared to control subjects.: This study highlights the importance of exposure to pesticides as an environmental risk factor for the development of breast cancer among women.

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CBD has taken the meaning of edibles to new heights. From oils, capsules, creams, gummy candy, and more, there is nothing CBD can’t be added to.

Marijuana brownies might have been popular in your dorm in college, but CBD brownies give you the same benefits without the (in many places) illegal high.

The combination of comforting, baked goods and the soothing benefits of CBD has led to the cannabidiol being added into cookies, cakes, brownies, and more throughout the country.

Interesting in trying it out on your own? Here is how to add CBD to baked goods

To use CBD in baking, the oil needs to be infused into a fat such as coconut oil or butter. Swap out the fat in the recipe with your CDB/fat mixture. If the CDB oil you are using already contains a base oil, you’re ready to go.

If you need to add your oil to fat, mix together, the CDB, water, and butter into a pan. Warm on low heat so the CDB does not bake out and let the mixture cool before using.

When cooking with CDB for the first time, stick with something you are comfortable with like a family cookie recipe or a boxed mix. Mistakes are less likely so you won’t waste your product.

Like the alcohol in rum cakes, CDB can bake out. Be mindful of temperature when your goods go in the oven and adjust cooking time as needed. The boiling point of CDB is 320-365 degrees Fahrenheit. Baking for too long or at a high heat can cause the CDB to evaporate and making your baking project ineffective.

Serving size is perhaps the most important aspect of cooking with CBD. For example, if you are cooking 24 cookies with 100 mg of CBD, each cookie will have 4mg of CDB. If you want more CBD in each serving, simply add more to the mix. To make sure you get all of the CDB added, make sure all of the batter is added by taking some extra time to scrap the bowl.

Once you’ve created your CDB baked goods, make sure to store them in a cool, dark place. CDB is light and heat sensitive and is at its maximum effectiveness when kept cool and dark. Also, keep your goodies in an air-tight container to keep them fresh.

PMID: 

Life Sci. 2018 May 1 ;200:81-86. Epub 2018 Mar 15. PMID: 29551577

Abstract Title: 

Association of prenatal organochlorine pesticide-dichlorodiphenyltrichloroethane exposure with fetal genome-wide DNA methylation.

Abstract: 

AIMS: To investigate whether intrauterine organochlorine pesticide (OCP)-dichlorodiphenyltrichloroethane (DDT) exposure could lead to epigenetic alterations by DNA methylation with possible important lifetime health consequences for offspring.MAIN METHODS: We used Illumina Infinium HumanMethylation 450 K BeadChip to explore the pattern of genome-wide DNA methylation containing>485,000 gene sites in cord blood of 24 subjects in a 12 mother-newborn pairs birth cohort. Based on the genome-wide DNA methylation data, we chose one potential gene, BRCA1, to verify the results in another group comprising 126 subjects.KEY FINDINGS: We identified 1,131 significantly different CpG sites which included 690 hypermethylation sites and 441 hypomethylation sites in the DNA methylation level between case and control group. The identified sites were located in 598 unique genes. In subsequent validation studies, we found that the DNA methylation level of the identified CpGs of BRCA1 increased with increased exposure to dichlorodiphenyltrichloroethane (DDT) and the level of gene expression in the identified CpGs of BRCA1 decreased with increased exposure to dichlorodiphenyltrichloroethane (DDT).SIGNIFICANCE: The results indicated that epigenetic processes played a possible role in the development of fetuses affected by maternal OCP-DDT exposure. Early prenatal exposure to DDT may affect fetal BRCA1 gene methylation, and increased exposure leads to a higher DNA methylation level and lower gene expression level.

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PMID: 

Front Endocrinol (Lausanne). 2019 ;10:122. Epub 2019 Mar 12. PMID: 30915030

Abstract Title: 

Oxidative Phosphorylation Impairment by DDT and DDE.

Abstract: 

There is increasing evidence supporting the characterization of the pesticide DDT and its metabolite, DDE, as obesogens and metabolic disruptors. Elucidating the mechanism is critical to understanding whether the association of DDT and DDE with obesity and diabetes is in fact causal. One area of research investigating the etiology of metabolic diseases is mitochondrial toxicity. Several studies have found associations between mitochondrial defects and insulin resistance, cellular respiration, substrate utilization, and energy expenditure. Although the mitotoxicity of DDT and DDE was established 20-40 years ago, it was not viewed in the light of the diseases faced today; therefore, it is prudent to reexamine the mitotoxicity literature for mechanistic support of DDT and DDE as causal contributors to obesity and diabetes, as well as associated diseases, such as cancer anddisease. This review aims to focus on studies investigating the effect of DDT or DDE on mammalian mitochondrial oxidative phosphorylation. We illustrate that both DDT and DDE impair the electron transport chain (ETC) and oxidative phosphorylation. We conclude that there is reasonable data to suggest that DDT and DDE target specific complexes and processes within the mitochondria, and that these insults could in turn contribute to the role of DDT and DDE in mitochondria-associated diseases.

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PMID: 

Environ Health Perspect. 2012 Aug ;120(8):1170-6. Epub 2012 Apr 18. PMID: 22514210

Abstract Title: 

Accelerated mammary tumor onset in a HER2/Neu mouse model exposed to DDT metabolites locally delivered to the mammary gland.

Abstract: 

BACKGROUND: The association of DDT (dichlorodiphenyltrichloroethane) with breast cancer is controversial, but animal studies directly linking DDT to risk are lacking. Concerns with DDT reside in its environmental persistence, bioaccumulation in breast adipose tissue, and endocrine-disrupting actions. Whereas most attention has been focused on estrogenic congeners, we tested the cancer-inducing potential of the antiandrogen, p,p´-DDE [1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene], the most prevalent and persistent DDT metabolite.OBJECTIVES: We aimed to determine whether developmental exposure to p,p´-DDE stored in adipose tissue surrounding the cancer-prone mammary epithelium of MMTV-Neu mice influences tumor development.METHODS: For localized delivery, Elvax 40P pellets containing p,p´-DDE were implanted into the mammary fat pads of prepubertal female mice. We compared mammary tumor development with p,p´-DDE with development in response to its estrogenic isomer, o,p´-DDE [1,1-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl) ethylene], and a mixture of both isomers.RESULTS: p,p´-DDE implants significantly accelerated mammary tumor onset compared with vehicle Elvax implants. o,p´-DDE had similar results, but only at ≤ 10 months of age. Lipid-adjusted levels of p,p´-DDE in mammary adipose tissue and serum in young mice were within the ranges of human exposure, whereasconcentrations in aged mice were low to undetectable. Exposure to a 2:1 ratio of p,p´-DDE:o,p´-DDE did not result in the younger latency observed with the individual isomers.CONCLUSIONS: p,p´-DDE exposure at concentrations relevant to human exposure accelerates mammary carcinogenesis in mice, possibly through hormonal and/or other actions. These data suggest that DDE exposure would promote, but not cause, mammary tumorigenesis. Developmental exposure in immature mammary tissue continues to affect tumor onset even after p,p´-DDE levels have declined. Future studies are needed to determine whether early exposure to p,p´-DDE correspondingly predisposes women to early-onset breast cancer.

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PMID: 

Arch Environ Contam Toxicol. 2019 Nov ;77(4):480-489. Epub 2019 Jul 19. PMID: 31324944

Abstract Title: 

Serum levels of Organochlorine Pesticides and Breast Cancer Risk in Iranian Women.

Abstract: 

Breast cancer is a multifactorial disease and its etiology is linked to multiple risk factors. There are shreds of controversial evidence that exposure to organochlorine pesticides (OCPs) are important in the etiology of breast cancer. The present study aimed to determine the circulating levels of OCPs in patients with breast tumors in Southeastern of Iran. This case-control study included 27 patients with malignant breast tumors (MBT), 31 patients with benign breast tumors (BBT), and 27 healthy women as a control group. Serum OCPs levels, includingα-hexachlorocyclohexane (α-HCH), β-HCH, γ-HCH, 2,4-dichlorodiphenyltrichloroethane (2,4-DDT), 4,4-DDT, 2,4-dichlorodiphenyldichloroethylene (2,4-DDE), and 4,4-DDE, were measured using gas chromatography. Our data revealed significantly higher concentrations of 2,4-DDT in MBT and BBT groups compared with control ones (P 

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PMID: 

Environ Int. 2018 12 ;121(Pt 2):1106-1112. Epub 2018 Oct 28. PMID: 30376997

Abstract Title: 

DDT exposure in early childhood and female breast cancer: Evidence from an ecological study in Taiwan.

Abstract: 

Researchers still lack consensus on the association between exposure to DDT and the risk of breast cancer. One reason could be that the measurements of DDT obtained during or near the time of diagnosis may not reflect exposure during the etiologically relevant time period in a woman's life. This study undertook an ecological analysis to investigate whether exposure to DDT among cohort born between 1951 and 1959 (i.e. age 0-5 years) and who reached the age 50-54 years during 2001-2013 had an increased risk of breast cancer in adulthood. To do this, we used the number of DDT sprays in each township during the anti-malaria campaign in Taiwan in the 1950s as a proxy for direct DDT exposure. The DDT sprays were then linked to the township female breast cancer incidence rate in the 2000s when the birth cohorts had reached age 50-54 years. Insurance claims data were used to identify breast cancer cases during 1996-2013. Zero-Inflated Poisson regression was performed to estimate the effect of DDT sprays on the breast cancer incidence rate. The analysis was based on a total of 9 birth cohorts (1951-1959) in 349 townships who had lived at least up to age 50. On average, one DDT spray experienced during age 0-5 years was associated with an increase of 8 more female breast cancer cases per 100,000 during age 50-54. The effect appears to increase with the number of sprays. Our finding suggests that DDT exposure in early childhood could raise the risk of breast cancer in adulthood.

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PMID: 

Mol Biol Rep. 2018 Dec ;45(6):1937-1945. Epub 2018 Nov 12. PMID: 30421125

Abstract Title: 

Expression of the miR-190 family is increased under DDT exposure in vivo and in vitro.

Abstract: 

A non-genotoxic insecticide dichlorodiphenyltrichloroethane (DDT), can affect mRNA and microRNA levels, however, its precise mechanism of action remains poorly understood. Using in silico methods we found that the rat miR-190 family is potentially regulated by CAR and ER receptors activated by DDT. We showed that exposure to DDT results in a dose- and organ-dependent increase in the expression of miR-190a, -190b in the liver, uterus, ovaries and mammary gland of female Wistar rats. Additionally, we demonstrate a decrease in protein product level of Tp53inp1, the target gene of these microRNAs, in the rat uterus. It is known that miR-190 is probably regulated by ER in humans, thus we measured the level of miR-190a, -190b in primary cultures of malignant and normal human endometrial cells treated with different doses of DDT. We detected an increase in miR-190b level in normal endometrial cells under DDT exposure. Thus, our results indicate that DDT exposure lead to change in the expression of oncogenic miR-190 family and its target gene Tp53inp1 which may be due to activation of CAR and ER.

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PMID: 

J Agric Food Chem. 2019 Nov 8. Epub 2019 Nov 8. PMID: 31703480

Abstract Title: 

Fluoride induces autoimmune orchitis involved with enhanced IL-17A secretion in mice testis.

Abstract: 

Fluoride (F) widely exists in the water and food. Recent studies reported that F induced testicular toxicity via inflammation reaction. This study was aimed to explore the mechanism of F-induced inflammation in testis. 100 healthy male mice (BALB/cJ strain) were randomly divided into five groups including: control, experimental autoimmune orchitis (EAO), and three F groups (25, 50 and 100 mg/L sodium fluoride (NaF)). After 150 d, the results showed a significant increase in testicular cytokines levels including of IL-17A, IL-6, IFN-γ and TNF-α in NaF and EAO groups compared with control group. Interestingly, the presence of specific anti-sperm autoantibodies in anti-testicular autoantibodies and the notable recruitment of immunocyte (T cells and dendritic cells) were also observed in NaF and EAO groups. In addition, findingsshowed that in NaF and EAO groups, macrophages and T cells both significantly secreted IL-17A, and the protein and mRNA levels of cytokines (IL-6 and TGF-β) were significantly increased. From these results, it can be concluded that autoimmune orchitis and IL-17A are implicated in F-induced testicular inflammation.

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PMID: 

Dev Biol. 2019 01 15 ;445(2):280-293. Epub 2018 Nov 27. PMID: 30500333

Abstract Title: 

Developmental origins of transgenerational sperm DNA methylation epimutations following ancestral DDT exposure.

Abstract: 

Epigenetic alterations in the germline can be triggered by a number of different environmental factors from diet to toxicants. These environmentally induced germline changes can promote the epigenetic transgenerational inheritance of disease and phenotypic variation. In previous studies, the pesticide DDT was shown to promote the transgenerational inheritance of sperm differential DNA methylation regions (DMRs), also called epimutations, which can in part mediate this epigenetic inheritance. In the current study, the developmental origins of the transgenerational DMRs during gametogenesis have been investigated. Male control and DDT lineage F3 generation rats were used to isolate embryonic day 16 (E16) prospermatogonia, postnatal day 10 (P10) spermatogonia, adult pachytene spermatocytes, round spermatids, caput epididymal spermatozoa, and caudal sperm. The DMRs between the control versus DDT lineage samples were determined at each developmental stage. The top 100 statistically significant DMRs at each stage were compared and the developmental origins of the caudal epididymal sperm DMRs were assessed. The chromosomal locations and genomic features of the different stage DMRs were analyzed. Although previous studies have demonstrated alterations in the DMRs of primordial germ cells (PGCs), the majority of the DMRs identified in the caudal sperm originated during the spermatogonia stages in the testis. Interestingly, a cascade of epigenetic alterations initiated in the PGCs is required to alter the epigenetic programming during spermatogenesis to obtain the sperm epigenetics involved in the epigenetic transgenerational inheritance phenomenon.

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