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pres.title = 'Endocrine-Disrupting Chemicals (EDCs)';

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// SLIDE 2 — TABLE OF CONTENTS
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  ["01", "INTRODUCTION", "Definition, history & global burden of EDCs"],
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  ["03", "MECHANISMS OF ACTION", "Nuclear receptors, nongenomic, epigenetic pathways"],
  ["04", "HUMAN EXPOSURE", "Routes, detection, vulnerable populations"],
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  ["06", "PREVENTION & CONCLUSIONS", "Strategies, guidelines, key takeaways"],
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// ============================================================
// ---- PART 1: INTRODUCTION ----
// ============================================================
addSectionDivider("INTRODUCTION", "What are Endocrine-Disrupting Chemicals?", "01");

// Slide 4 — Definition & Scope
contentSlide("What Are Endocrine-Disrupting Chemicals (EDCs)?", [
  "EDCs are exogenous agents that disrupt normal endocrine physiology by interfering with hormone synthesis, metabolism, and/or cellular actions.",
  "They possess estrogenic, anti-estrogenic, androgenic, anti-androgenic, and other hormonal effects.",
  "EDCs are found in air, water, soil, household products, personal care products, and medical devices — making them ubiquitous in the environment.",
  "Over 1,000 individual EDCs have been identified (The Endocrine Disruptor Exchange – TEDX).",
  "EDCs can cross the placenta and are implicated in the developmental origins of obesity, diabetes, cancer, and infertility.",
  "Epidemiologic data suggest the rise in diabetes, cancer, and infertility over the past 2–3 decades may be partly attributable to in utero EDC exposure.",
  "EDCs are also recognised as a significant contributor to climate change, contaminating ecosystems worldwide.",
]);

// Slide 5 — Historical Context
contentSlide("Historical Context", [
  "EDCs first gained widespread attention due to their effects on abnormal development of fish, aquatic animals, and birds following high-level industrial contamination.",
  "Early studies on high-level exposures were largely dismissed as irrelevant to human exposure levels.",
  "Landmark: Diethylstilbestrol (DES) was prescribed to prevent miscarriage (1940s–1970s) and caused significant reproductive abnormalities and rare cancers in offspring — the most compelling early human evidence.",
  "Today, a robust body of evidence from epidemiologic, animal, and cell-based studies confirms that even low-level real-world exposures matter for human health.",
  "The Endocrine Society issued its first major Scientific Statement on EDCs in 2009 (Diamanti-Kandarakis et al.), followed by the EDC-2 statement in 2015.",
  "Global regulatory response: The European Union has banned certain EDC-containing products; the US and WHO have updated guidelines.",
]);

// Slide 6 — Types of EDCs
twoColSlide(
  "Types of Endocrine-Disrupting Chemicals",
  [
    "Plant-derived (Phytoestrogens): genistein, daidzein — found in flaxseed, soy, legumes",
    "Industrial chemicals: pesticides, flame retardants (PFAS), combustion products (PAHs, dioxins), lubricants (PCBs)",
    "Medical supplies: IV tubing, gloves, bags — contain BPA and phthalates",
    "Pharmaceuticals: DES, synthetic and natural steroids, estradiol",
  ],
  [
    "Household & personal care items: cosmetics, sunscreens, hair relaxers, toys",
    "Food/beverage packaging: BPA, phthalates, perchlorate, dioxins",
    "Water & environmental contaminants: PFAS chemicals in groundwater, DDT in soil",
    "Tobacco products, tea tree & lavender oils (weak estrogenic/anti-androgenic activity)",
    "Benzophenone-3 / oxybenzone in sunscreens — identified EDC; substantial systemic absorption",
  ],
  "Natural / Pharmaceutical Sources",
  "Industrial / Consumer Sources"
);

// ============================================================
// ---- PART 2: MECHANISMS OF ACTION ----
// ============================================================
addSectionDivider("MECHANISMS OF ACTION", "How do EDCs alter endocrine physiology?", "02");

// Slide 8 — Classic Nuclear Receptor Pathway
contentSlide("Mechanism 1: Classic Nuclear Receptor Pathway", [
  "The most established mechanism: EDCs activate or inhibit nuclear receptor (NR) signaling.",
  "Nuclear hormone receptors are ligand-modulated transcription factors that interact with DNA response elements within target genes.",
  "EDCs bind to the ligand-binding pockets of receptors for estrogens (ERα, ERβ), androgens (AR), progestins (PR), and thyroid hormone (TR).",
  "Glucocorticoid/mineralocorticoid receptor (GR/MR) systems are also targets of EDCs.",
  "EDCs recruit coactivator or corepressor proteins to DNA response elements, activating or repressing gene expression.",
  "Most EDCs bind with >1,000-fold lower affinity than endogenous hormones — suggesting alternative pathways play a critical role at physiologic doses.",
  "Example: BPA mimics estradiol and activates ERα/ERβ, disrupting reproductive gene programs.",
]);

// Slide 9 — Nongenomic Signaling
contentSlide("Mechanism 2: Nongenomic Nuclear Receptor Signaling", [
  "EDCs can activate nongenomic (membrane-level) signaling independently of nuclear receptor transcription.",
  "Key receptor: GPR30 (seven-transmembrane ER) — a membrane-bound estrogen receptor that triggers rapid intracellular signaling cascades.",
  "Genistein and BPA possess GREATER relative binding affinity for GPR30 compared with estradiol.",
  "Both activate GPR30 with similar efficacy as estradiol at concentrations of 1 pM–1 nM.",
  "BPA detected at nM concentrations in human fetal serum, breast milk, amniotic fluid, and cord blood — sufficient to activate GPR30.",
  "Rapid downstream effects include Ca²⁺ flux, MAPK/ERK activation, and prolactin release.",
  "This mechanism likely explains estrogenic effects of BPA observed at environmentally relevant exposures.",
]);

// Slide 10 — Epigenetic Effects
contentSlide("Mechanism 3: Epigenetic Reprogramming", [
  "The epigenome consists of chemical modifications (methylation, acetylation) that control how genes respond to environmental cues.",
  "Critical window: prenatal and early postnatal periods — epigenetic modifications (histone methylation, CpG methylation) are actively established.",
  "Early EDC exposure can induce DEVELOPMENTAL REPROGRAMMING — lasting epigenetic changes with potential for transgenerational transmission.",
  "DES exposure during pregnancy: significant reproductive abnormalities and rare cancers in offspring, via epigenetic reprogramming.",
  "BPA and other EDCs may increase susceptibility to chronic diseases in adulthood (endocrine disorders, diabetes, cancer) via early epigenetic changes.",
  "Mechanism in prostate cancer: EDCs activate histone methyltransferase MLL1, altering methylation patterns during prostate development — changes persisting to adulthood, elevating cancer risk.",
  "PAH exposure in utero: altered methylation of PPAR-γ (primary regulator of adipogenesis) — mechanistic link to obesity.",
]);

// Slide 11 — Additional Mechanisms
twoColSlide(
  "Additional Mechanisms of EDC Action",
  [
    "Hormone biosynthesis disruption: Phthalates & pesticides inhibit steroidogenic enzymes (e.g., CYP19A1 aromatase), reducing estradiol production.",
    "Steroid transport disruption: PCBs, BPA, and genistein bind thyroid transport proteins, altering free vs. bound thyroid hormone ratio.",
    "Metabolic enzyme induction: CYP1B1-mediated hormone catabolism is increased by phthalates and pesticides.",
    "Kisspeptin pathway interference: EDCs disrupt hypothalamic kisspeptin → impaired GnRH pulse generation → altered LH/FSH release.",
  ],
  [
    "Mixture / synergistic effects: EDCs rarely act alone; mixtures produce additive or synergistic effects — demonstrated in breast, ovarian, and prostate cells.",
    "Non-linear dose-response: EDCs frequently do NOT follow traditional linear dose-response; effects seen at very low exposures, especially during critical windows (in utero, puberty).",
    "Adipose accumulation: Lipophilic EDCs accumulate in fat tissue and are released into bloodstream over time, prolonging exposure.",
    "No established safe dose: The Endocrine Society states that no safe dose of EDC exposure can be assumed, especially during vulnerable developmental windows.",
  ],
  "Hormonal Pathway Disruption",
  "Dose & Mixture Effects"
);

// ============================================================
// ---- PART 3: HUMAN EXPOSURE ----
// ============================================================
addSectionDivider("HUMAN EXPOSURE", "Routes, detection & vulnerable populations", "03");

// Slide 13 — Routes & Detection
contentSlide("Routes of Exposure & Biomonitoring", [
  "Ingestion: contaminated food, water, dust (major route — packaging, seafood, produce)",
  "Inhalation: gases, particles, combustion by-products (PAHs, flame retardants) in air",
  "Dermal contact: personal care products, cosmetics, topical creams",
  "Placental transfer: EDCs cross the placenta — high levels found in amniotic fluid and umbilical cord blood",
  "Breast milk: numerous EDCs detected; neonates receive exposure through feeding",
  "NHANES 2003–2004: Detectable BPA in 93% of urine samples from individuals ≥6 years (CDC)",
  "Survey of 1,000 individuals: majority tested positive for phthalates (plasticizers in household, medical & cosmetic products)",
  "PFAS chemicals: ubiquitous in blood of humans worldwide",
  "EDCs detected in human blood, sweat, urine, breast milk, and hair — in both children and adults",
]);

// ============================================================
// ---- PART 4: HEALTH EFFECTS ----
// ============================================================
addSectionDivider("HEALTH EFFECTS", "Reproductive, metabolic, neurologic & oncologic impacts", "04");

// Slide 15 — Reproductive Effects (Female)
twoColSlide(
  "Reproductive Effects: Women & Children",
  [
    "Precocious puberty: EDCs (lavender/tea tree oils, phthalates, DDT metabolite p,p'-DDE) linked to early puberty, premature thelarche, gynecomastia in boys.",
    "Ovarian toxicity: BPA associated with ovarian cysts, follicle atresia, impaired implantation in IVF.",
    "Fertility: BPA, phthalates, pesticides, PCBs disrupt folliculogenesis, ovulation, and fertilization.",
    "Steroidogenesis: Phthalates/pesticides inhibit estradiol production; BPA alters estradiol, testosterone, and pregnenolone in granulosa/thecal cells.",
    "PCOS: Higher serum BPA in women with PCOS; correlates with hyperandrogenemia and insulin resistance.",
  ],
  [
    "Endometriosis: Dioxin stimulates uterine epithelial growth; EDCs act on estrogen-dependent lesions and immune system.",
    "Uterine fibroids: DES daughters have higher fibroid risk; epigenetic reprogramming by DES and genistein increases myometrial hormone sensitivity.",
    "Testicular Dysgenesis Syndrome (TDS): EDC-linked triad — abnormal fetal testis development, decreased semen quality, testicular germ cell cancer.",
    "Male fertility: DDT exposure → reduced sperm volume, concentration, motility, morphology; BPA exposure → decline in sperm quality; PCBs inversely correlated with sperm motility.",
    "Phthalates: Anti-androgenic effects; phthalate capsule exposure in IBD patients reduced LH, FSH, testosterone, and inhibin B.",
  ],
  "Female Reproductive Effects",
  "Male & Pediatric Effects"
);

// Slide 16 — Metabolic & Systemic Effects
contentSlide("Metabolic, Cardiovascular & Respiratory Effects", [
  "Obesity ('obesogens'): BPA, phthalates, tributyltin (TBT) promote adipogenesis. Phthalate exposure estimated to contribute to ~54,000 obesity cases in older European women.",
  "Diabetes: BPA linked to insulin resistance and type 2 diabetes in women of reproductive age; urinary phthalate metabolites increase diabetes incidence across all ages.",
  "PCOS & metabolic overlap: TBT induces PCOS-like features (reproductive, metabolic, cardiovascular) in animal models.",
  "MASLD (metabolic liver disease): PCBs and PFAS exposure associated with increased liver dysfunction and MASLD phenotypes — affecting ~30–40% of the world population.",
  "Cardiovascular: BPA exposure linked to coronary artery disease and hypertension (meta-analysis, 33 studies); maternal BPA in 2nd trimester predicts elevated diastolic BP at age 4.",
  "Respiratory: Over 50 EDCs — including BPA, phthalates, benzophenone-3 — found in household products and associated with asthma; PVC/phthalates linked to asthma/allergy in children.",
  "Childhood obesity: PFAS chemicals increasingly recognised as risk factor for obesity in children and adolescents.",
]);

// Slide 17 — Neurological Effects
contentSlide("Neurological & Thyroid Effects", [
  "Neurodevelopmental deficits: Prenatal glycol ether exposure → neurocognitive deficits in 6-year-olds (PELAGIE cohort); prenatal insecticide → cognitive difficulties and abnormal social behaviour.",
  "Academic performance: EDC exposure (BPA, phthalates) linked to lower grade-point averages in children; PCBs in utero linked to lower IQ.",
  "ASD & ADHD: EDCs express autism-associated genes; organochloride pesticides near agriculture → 6× increased ASD risk; ADHD-related behaviours associated with higher urinary phthalates in adolescents.",
  "Thyroid disruption: EDCs impact thyroid hormone biosynthesis, transport, metabolism, and TR activity. Even mild maternal thyroid fluctuations impair fetal neurodevelopment.",
  "PBDEs (flame retardants): Associated with hypothyroidism (prevalence ratio 1.7).",
  "Perchlorate: Inhibits iodide transporter — disrupts T3/T4 biosynthesis; inversely correlated with offspring cognitive ability in pregnant women with borderline thyroid function.",
  "PFAS: Disrupt multiple steps in thyroid hormone synthesis; associated with abnormal thyroid function in infants, children, and adults.",
]);

// Slide 18 — Cancer
contentSlide("Hormone-Related Cancers", [
  "Breast cancer: Excess estrogen in utero → elevated breast cancer incidence. DES daughters ≥40 years: 2.1× greater breast cancer incidence. Prenatal DDT exposure → ~4× increased risk in daughters (longitudinal study).",
  "Hair products & breast cancer: In a study of >50,000 US/Puerto Rico women, hair dye and straightener use associated with increased breast cancer risk (especially African American women). >5,000 chemicals in hair products, some known EDCs.",
  "Endometrial & ovarian cancer: Hair straightener chemicals (phenols, phthalates, parabens, cyclosiloxanes) linked to increased incidence in epidemiologic studies.",
  "Prostate cancer: Occupational pesticide exposure (Agricultural Health Study, ~90,000 participants) directly correlated with prostate cancer incidence. Arsenic, cadmium, PCBs also implicated.",
  "Prostate cancer mechanism: EDCs with estrogenic activity initiate prostatic carcinogenesis in androgen-supported environment; epigenetic changes in prostate tumor stroma promote malignant invasiveness.",
  "Testicular cancer (TGCC): Rising incidence over past decades. Serum DDE levels correlated with both seminomatous and nonseminomatous TGCC risk (case-control, n=754).",
  "Phytoestrogens: Genistein and resveratrol may have anti-tumorigenic effects in some experimental systems by dampening ER stimulatory activity.",
]);

// ============================================================
// ---- PART 5: PREVENTION & CONCLUSIONS ----
// ============================================================
addSectionDivider("PREVENTION & CONCLUSIONS", "Reducing exposure & key clinical takeaways", "05");

// Slide 20 — Prevention Strategies
twoColSlide(
  "Prevention of EDC Exposure: Practical Strategies",
  [
    "BPA: Use BPA-free products and glass for food storage/cooking. Especially critical for infants, children, and pregnant women. EU recommends 20,000-fold reduction in tolerable daily BPA intake.",
    "Phthalates: Use filtered water; avoid plastics in food prep; choose fragrance-free soaps, detergents, and cosmetics.",
    "Sunscreens: Use mineral-based (titanium dioxide, zinc oxide) over chemical filters; avoid oxybenzone (benzophenone-3 / BP-3).",
    "PFAS: Test well water annually; use NSF/ANSI certified filters, especially during pregnancy. Avoid coastal European seafood (high EDC contamination).",
  ],
  [
    "Dioxins: Replace bleached paper products (diapers, towels, tissues) with cloth alternatives.",
    "Pesticides: Peel produce or soak 15 min in baking soda (sodium bicarbonate) solution to significantly reduce pesticide residues.",
    "Topical products for children: Avoid tea tree and lavender oil formulations (estrogenic/anti-androgenic); consult paediatrician/pharmacist before use.",
    "DES-exposed individuals: Regular screening for reproductive malignancies if exposed in utero.",
    "Clinical communication: Inform patients about EDC exposure risks and guide lifestyle changes to reduce exposure, especially during pregnancy and childhood.",
  ],
  "Individual / Consumer Strategies",
  "Clinical & Regulatory Guidance"
);

// Slide 21 — Conclusion
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const conclusions = [
  ["Definition", "EDCs are exogenous agents disrupting hormone synthesis, metabolism, and/or cellular actions — with estrogenic, anti-estrogenic, androgenic, anti-androgenic, and other hormonal effects."],
  ["Mechanisms", "EDCs act via nuclear receptors, nongenomic GPR30 signaling, and epigenetic reprogramming — often at very low (picomolar–nanomolar) doses without a definable safe threshold."],
  ["Exposure", "EDCs are ubiquitous — detected in 93% of urine samples (BPA), virtually all adults (PFAS, phthalates). Placental transfer places the developing fetus at highest risk."],
  ["Health Impact", "EDCs are linked to reproductive disorders (PCOS, infertility, TDS), metabolic disease (obesity, diabetes), hormone-sensitive cancers, neurological deficits, thyroid dysfunction, and CVD."],
  ["Clinical Action", "Clinicians should counsel patients — especially pregnant women, infants, and children — on EDC reduction strategies. No safe exposure level is established."],
];

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  conc.addShape(pres.ShapeType.rect, { x: 1.95, y: y + 0.12, w: 0.04, h: 0.54, fill: { color: ACCENT } });
});

conc.addShape(pres.ShapeType.rect, { x: 0, y: 5.57, w: 10, h: 0.055, fill: { color: ACCENT } });

// ============================================================
// WRITE FILE
// ============================================================
pres.writeFile({ fileName: "/home/daytona/workspace/edc-presentation/EDC_Presentation.pptx" })
  .then(() => console.log("SUCCESS: EDC_Presentation.pptx created"))
  .catch(e => console.error("ERROR:", e));