Le sostanze chimiche sintetiche che possono raggiungere ed alterare la normale omeostasi endocrina tramite l'esposizione alimentare o tramite l'ambiente esterno, agiscono sugli ormoni steroidei modulando in modo reversibile l'attività ormonale o causando danni. La loro azione è diretta, a causa del legame con i recettori degli androgeni, degli estrogeni e degli ormoni tiroidei (1). 

Poiché sistema endocrino è per sua natura sensibile e dinamicamente modulato sul rapporto dose-risposta, è importante soffermarsi sulla quantità delle sostanze che potrebbero causare danni al sistema.

Gli  interferenti endocrini (EDS) sono definiti dall'Organizzazione mondiale della sanità "an endocrine disruptor is an exogenous substance or mixture that alters function(s) of the endocrine system and consequently causes adverse health effects in an intact organism, or its progeny, or (sub)populations".

Tra gli  interferenti endocrini più comuni, i pesticidi sono i più diffusi e dal 1939, anno della scoperta del DDT, le industrie chimiche hanno prodotto in quantità massiccia una miriade di sostanze per difenderci da insetti, roditori, funghi, erbe infestanti e parassiti (2).

Oltre alla pericolosità immediata e diretta, i pesticidi possono rimanere sul terreno, esercitando la loro azione, per molto tempo, penetrare nel terreno inquinando le acque, insediarsi nei vertebrati ed invertebrati e, tramite questi ultimi, risalire ai predatori.

Alcuni interferenti endocrini possono agire sul DNA, altri possono disturbare lo sviluppo riproduttivo, altri hanno un collegamento con il cancro alla prostata, ma gli studi sono a volte contrastanti in quanto giocano come cofattori, l'età, il sesso, la durata dell'esposizione e, come dicevamo prima, le quantità.

I Parabeni sono composti chimici conservanti che sono stati oggetto di attenzione da parte della letteratura scientifica quali possibili interferenti endocrini (in particolare propylparaben e butiylparabene) cioè con possibilità di danneggiare le ghiandole del nostro corpo che producono ormoni, in particolare nel seno. Lo studio di Darbre ed altri del 2004 poneva in evidenza come i parabeni rimangano nel nostro corpo come esteri intatti. Dopo questo studio, una parte della letteratura scientifica, nel 2005 e nel 2006, ha sollevato dubbi sulle conclusioni di Darbre sostenendone la limitatezza. Tuttavia, sia la FDA statunitense che l'SCCP europeo hanno autorizzato nel 2006 l'uso di un parabene singolo in prodotti cosmetici nella concentrazione dello 0,4% e l'uso di parabeni totali nella concentrazione di 0,8%. Non mancano comunque gli studi che ritengono inutili le limitazioni: M. G. Kirchhof ed altri, nel 2013, ritiene che i parabeni siano tra i conservanti più sicuri e ben tollerati e che i dati attuali non supportino  regolamenti drastici o restrizioni personali all'esposizione. Nel 2014 Darbre ha pubblicato un ulteriore studio in cui ha dimostrato come i parabeni possano causare danni al DNA e nel 2017 un altro studio sul rapporto tra parabeni, regolazione endocrina del metabolismo energetico e struttura del tessuto adiposo.

L'alternativa è rappresentata dai prodotti naturali.

Bibliografia_____________________________________________________________________

(1) Tabb MM, Blumberg B. New modes of action for endocrine-disrupting chemicals. Mol Endocrinol. 2006 Mar;20(3):475-82. doi: 10.1210/me.2004-0513. 

Abstract. Endocrine-disrupting chemicals (EDC) are commonly considered to be compounds that mimic or block the transcriptional activation elicited by naturally circulating steroid hormones by binding to steroid hormone receptors. For example, the Food Quality Protection Act of 1996 defines EDC as those, that "may have an effect in humans that is similar to an effect produced by a naturally occurring estrogen, or other such endocrine effect as the Administrator may designate." The definition of EDC was later expanded to include those that act on the estrogen, androgen, and thyroid hormone receptors. In this minireview, we discuss new avenues through which xenobiotic chemicals influence these and other hormone-dependent signaling pathways. EDC can increase or block the metabolism of naturally occurring steroid hormones and other xenobiotic chemicals by activating or antagonizing nuclear hormone receptors. EDC affect the transcriptional activity of nuclear receptors by modulating proteasome-mediated degradation of nuclear receptors and their coregulators. Xenobiotics and environmental contaminants can act as hormone sensitizers by inhibiting histone deacetylase activity and stimulating mitogen-activated protein kinase activity. Some endocrine disrupters can have genome-wide effects on DNA methylation status. Others can modulate lipid metabolism and adipogenesis, perhaps contributing to the current epidemic of obesity. Additional elucidation of these new modes of endocrine disruption will be key in understanding the nature of xenobiotic effects on the endocrine system.

(2) Andersen HR, Vinggaard AM, Rasmussen TH, Gjermandsen IM, Bonefeld-Jørgensen EC. Effects of currently used pesticides in assays for estrogenicity, androgenicity, and aromatase activity in vitro. Toxicol Appl Pharmacol. 2002 Feb 15;179(1):1-12. doi: 10.1006/taap.2001.9347. 

Abstract. Twenty-four pesticides were tested for interactions with the estrogen receptor (ER) and the androgen receptor (AR) in transactivation assays. Estrogen-like effects on MCF-7 cell proliferation and effects on CYP19 aromatase activity in human placental microsomes were also investigated. Pesticides (endosulfan, methiocarb, methomyl, pirimicarb, propamocarb, deltamethrin, fenpropathrin, dimethoate, chlorpyriphos, dichlorvos, tolchlofos-methyl, vinclozolin, iprodion, fenarimol, prochloraz, fosetyl-aluminum, chlorothalonil, daminozid, paclobutrazol, chlormequat chlorid, and ethephon) were selected according to their frequent use in Danish greenhouses. In addition, the metabolite mercaptodimethur sulfoxide, the herbicide tribenuron-methyl, and the organochlorine dieldrin, were included. Several of the pesticides, dieldrin, endosulfan, methiocarb, and fenarimol, acted both as estrogen agonists and androgen antagonists. Prochloraz reacted as both an estrogen and an androgen antagonist. Furthermore, fenarimol and prochloraz were potent aromatase inhibitors while endosulfan was a weak inhibitor. Hence, these three pesticides possess at least three different ways to potentially disturb sex hormone actions. In addition, chlorpyrifos, deltamethrin, tolclofos-methyl, and tribenuron-methyl induced weak responses in one or both estrogenicity assays. Upon cotreatment with 17beta-estradiol, the response was potentiated by endosulfan in the proliferation assay and by pirimicarb, propamocarb, and daminozid in the ER transactivation assay. Vinclozolin reacted as a potent AR antagonist and dichlorvos as a very weak one. Methomyl, pirimicarb, propamocarb, and iprodion weakly stimulated aromatase activity. Although the potencies of the pesticides to react as hormone agonists or antagonists are low compared to the natural ligands, the integrated response in the organism might be amplified by the ability of the pesticides to act via several mechanism and the frequent simultaneous exposure to several pesticides.

(3) Darbre PD. Endocrine Disruptors and Obesity. Curr Obes Rep. 2017 Mar;6(1):18-27. doi: 10.1007/s13679-017-0240-4. PMID: 28205155; PMCID: PMC5359373.

Abstract. Purpose of review: The purpose of this review was to summarise current evidence that some environmental chemicals may be able to interfere in the endocrine regulation of energy metabolism and adipose tissue structure. Recent findings: Recent findings demonstrate that such endocrine-disrupting chemicals, termed "obesogens", can promote adipogenesis and cause weight gain. This includes compounds to which the human population is exposed in daily life through their use in pesticides/herbicides, industrial and household products, plastics, detergents, flame retardants and as ingredients in personal care products. Animal models and epidemiological studies have shown that an especially sensitive time for exposure is in utero or the neonatal period. In summarising the actions of obesogens, it is noteworthy that as their structures are mainly lipophilic, their ability to increase fat deposition has the added consequence of increasing the capacity for their own retention. This has the potential for a vicious spiral not only of increasing obesity but also increasing the retention of other lipophilic pollutant chemicals with an even broader range of adverse actions. This might offer an explanation as to why obesity is an underlying risk factor for so many diseases including cancer.