[10] DEHP is a component of many household items, including tablecloths, floor tiles, shower curtains, garden hoses, rainwear, dolls, toys, shoes, medical tubing, furniture upholstery, and swimming pool liners.

Common exposures come from the use of DEHP as a fragrance carrier in cosmetics, personal care products, laundry detergents, colognes, scented candles, and air fresheners.

[12] DEHP levels in some European samples of milk, were found at 2000 times higher than the EPA Safe Drinking Water limits (12,000 ppb).

According to the European Commission Scientific Committee on Health and Environmental Risks (SCHER), exposure to DEHP may exceed the tolerable daily intake in some specific population groups, namely people exposed through medical procedures such as kidney dialysis.

DEHP, along with other phthalates, is believed to cause endocrine disruption in males, through its action as an androgen antagonist,[22] and may have lasting effects on reproductive function, for both childhood and adult exposures.

The claims have received support by a study[25] using dogs as a "sentinel species to approximate human exposure to a selection of chemical mixtures present in the environment".

DEHP exposure during pregnancy has been shown to disrupt placental growth and development in mice, resulting in higher rates of low birthweight, premature birth, and fetal loss.

[26] In a separate study, exposure of neonatal mice to DEHP through lactation caused hypertrophy of the adrenal glands and higher levels of anxiety during puberty.

[27] In another study, pubertal administration of higher-dose DEHP delayed puberty in rats, reduced testosterone production, and inhibited androgen-dependent development; low doses showed no effect.

This is observed in conjunction with a significant decrease in the amount of expression and instability of gap junctional connexin proteins, specifically connexin-43, in cardiomyocytes treated with DEHP.

[31] The decrease in expression and instability of connexin-43 may be due to the down regulation of tubulin and kinesin genes, and the alteration of microtubule structure, caused by DEHP; all of which are responsible for the transport of protein products.

[32] DEHP has also been shown, in vitro using cardiac muscle cells, to cause activation of PPAR-alpha gene, which is a key regulator in lipid metabolism and peroxisome proliferation; both of which can be involved in atherosclerosis and hyperlipidemia, which are precursors of cardiovascular disease.

[33] Once metabolized into MEHP, the molecule has been shown to lengthen action potential duration and slow epicardial conduction velocity in Langendorff perfused rodent hearts.

[37] In October 2009, Consumers' Foundation, Taiwan (CFCT) published test results[38] that found 5 out of the sampled 12 shoes contained over 0.1% of phthalate plasticizer content, including DEHP, which exceeds the government's Toy Safety Standard (CNS 4797).

[40] The Department of Health confirmed that contaminated food and beverages had been exported to other countries and regions, which reveals the widespread prevalence of toxic plasticizers.

[41] In 2005, the Council and the Parliament compromised to propose a ban on three types of phthalates (DINP, DIDP, and DNOP) "in toys and childcare articles which can be placed in the mouth by children".

[42] In 2008, six substances were considered to be of very high concern (SVHCs) and added to the Candidate List including musk xylene, MDA, HBCDD, DEHP, BBP, and DBP.

[44] In 2012, Danish Environment Minister Ida Auken announced the ban of DEHP, DBP, DIBP and BBP, pushing Denmark ahead of the European Union which has already started a process of phasing out phthalates.

DEHP is classified as a "chemical known to the State of California to cause cancer and birth defects or other reproductive harm" (in this case, both) under the terms of Proposition 65.