I think his point is that the FDA finds that there is no evidence to support this claim. What evidence do you have that this claim is true?
There have been a number of papers from China showing that phthalate exposure from household dust is a real concern (e.g., https://pubmed.ncbi.nlm.nih.gov/35508265/).
Phthalate exposure overall has been shown to have an adverse impact on reproductive health and infertility, metabolic and oxidative stress, cancer risk, cardiovascular health, the immune system (including children’s asthma), and neurodevelopment. Unlike dietary studies which often have mixed results, the conclusions on phthalate exposure are consistently negative.
No idea what the FDA is doing here. I understand government inertia but they seem asleep at the wheel.
Do you see the drugs they approved for AD? These drugs all cause deadly brain bleeds by removing beta amyloid which is not even the cause of AD. There is no way that these drugs fix AD. Yet, they will make the drug makers pretty rich.
The FDA seems to have an internal mandate that no fixes are to be instituted if someone is not making continuously making a load from it, at least until the first few generations of patents have expired.
"If you pay me enough in speaker's fees, I'll approve any chemical you want!"
"If you promise me a comfy corporate job after I put in my time here, I will do anything you want!"
Phthalates and Their Impacts on Human Health (2021)
> phthalates are more likely to enter the body through absorption via the skin and the polluted air due to fugitive emission [10]. Phthalates are semi-volatile organic compounds (SVOCs). DEHP and DBP are the main compounds in both indoor and outdoor air phthalates [11]. Dermal absorption also occurs from the daily use of PCPs containing phthalates via plastic package. Infants are exposed to phthalates by drinking breast milk with their mothers exposed to DEHP and DiNP, and sucking on toys containing DEHP, DBP, and BBP [10]. Phthalates are also found to cross the placenta-blood barrier, which is the major exposure route of the fetus [12].
> Studies found that low molecular phthalates, such as DEP, can acutely irritate the skin, conjunctiva, and mucous membrane of the oral and nasal cavities [20]. Phthalate exposure is associated with adverse developmental effects in terms of increased prenatal mortality, reduced growth and birth weight, skeletal, visceral, and external malformations in rodents [6]. Experiments on male rats found that the nervous system is rather sensitive to low doses of DEHP exposure during puberty [21]. The impacts of phthalates on human beings vary from gene expression to physiological changes. High molecular weight phthalates exposure is found to cause methylation status of imprinted genes, which could be directly related to androgen response, estrogen response, protein secretion, and spermatogenesis [22,23]. Human epidemiological studies have shown a significant association between phthalates exposures and adverse reproductive outcomes in both women and men, for instance, type II diabetes and insulin resistance, overweight/obesity, allergy, asthma [24].
Exposure to the plasticizer dibutyl phthalate causes oxidative stress and neurotoxicity in brain tissue (2024)
> The induction of oxidative stress in the brain subcellular fractions was proved by alterations in the activities of superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase along with the reduction in the total antioxidant capacity. Meanwhile, the levels of hydrogen peroxide and lipid peroxidation were increased. Neurotransmitters such as acetylcholine, dopamine, adrenaline, noradrenaline, and serotonin were altered in all subcellular fractions suggesting the disruption of the neurotransmitter system in the fish brain. These results indicate that DBP induces oxidative stress, which correlates with neurotoxicity in Pseudetroplus maculatus brain tissue.
Microplastics and phthalate esters release from teabags into tea drink: occurrence, human exposure, and health risks (2023)
> DEHP showed the cancer risk (CR) for children and adults. The findings of this research indicated that high MPs and PAEs levels are released from teabags into tea drinks. Considering a daily drinking of a volume of 150 and 250 mL tea by children and adults, 486 and 810 MPs may enter their bodies, respectively. Thus, tea prepared with teabag-packed herbs may pose a significant health risk for consumers.
Preconception Phthalate Exposure and Women's Reproductive Health: Pregnancy, Pregnancy Loss, and Underlying Mechanisms (2023)
> Results: An interquartile range (IQR) higher mono-(2-ethylhexyl) phthalate [fecundability odds ratio(FOR)=0.88; 95% confidence interval (CI): 0.78, 1.00], mono-butyl phthalate (FOR=0.82; 95% CI: 0.70, 0.96), and mono-benzyl phthalate (FOR=0.85; 95% CI: 0.74, 0.98) was associated with lower fecundability. No consistent associations were observed with pregnancy loss. Preconception phthalates were consistently associated with higher hsCRP and isoprostanes, as well as lower estradiol and higher follicle-stimulating hormone across the menstrual cycle.
> Discussion: Women's preconception exposure to phthalates was associated with lower fecundability, changes in reproductive hormones, and increased inflammation and oxidative stress. The pre- and periconception periods may represent sensitive windows for intervening to limit the reproductive toxicity of phthalate exposure.
Maternal phthalate exposure promotes allergic airway inflammation over 2 generations through epigenetic modifications (2018)
> Results: In LINA maternal urinary concentrations of mono-n-butyl phthalate, a metabolite of butyl benzyl phthalate (BBP), were associated with an increased asthma risk in the children. Using a murine transgenerational asthma model, we demonstrate a direct effect of BBP on asthma severity in the offspring with a persistently increased airway inflammation up to the F2 generation. This disease-promoting effect was mediated by BBP-induced global DNA hypermethylation in CD4+ T cells of the offspring because treatment with a DNA-demethylating agent alleviated exacerbation of allergic airway inflammation. Thirteen transcriptionally downregulated genes linked to promoter or enhancer hypermethylation were identified. Among these, the GATA-3 repressor zinc finger protein 1 (Zfpm1) emerged as a potential mediator of the enhanced susceptibility for TH2-driven allergic asthma.
> Conclusion: These data provide strong evidence that maternal BBP exposure increases the risk for allergic airway inflammation in the offspring by modulating the expression of genes involved in TH2 differentiation through epigenetic alterations.
From Oxidative Stress to Male Infertility: Review of the Associations of Endocrine-Disrupting Chemicals (Bisphenols, Phthalates, and Parabens) with Human Semen Quality (2022)
> Higher levels of urinary bisphenols showed correlation with impaired semen quality and increased DNA damage. Considering phthalates and their metabolites, all studies found a positive association between urinary levels of phthalates and at least one semen parameter indicative of low semen quality; some studies also revealed sperm DNA damage. The studies on parabens less often revealed correlation of urinary parabens concentrations with a decrease in sperm count, as well as motility and DNA damage. Moreover, EDCs can elevate ROS production and lipid peroxidation, increase apoptosis, induce epigenetic modifications, and change the Y:X sperm chromosome ratio and sperm protein composition. Our review revealed detrimental effects of EDCs on semen quality and sperm DNA integrity—especially in BPA and phthalates, but also in parabens.
Can phthalates impair liver function? (2019)
> Conclusions: The ubiquitous exposure to phthalates may be related to the impairment of normal liver function
