Health and Environment
Health and Environmental Impacts of DEHP
Human and environmental health impacts may result when exposure to DEHP occurs. The following is a brief summary of potential exposure routes and the associated human and environmental health impacts. As scientific research evolves new information on these impacts will likely emerge. Readers are therefore encouraged to consult the references for updates.
Human exposure to DEHP during manufacture or consumer use occurs primarily through:
- Inhalation, particularly during manufacture and processing
- Oral exposure (primarily a product-related concern), or
- Injection during medical procedures, especially when high lipid content medical fluids directly contact DEHP-containing materials.
Because DEHP has a low vapor pressure, when present in product relatively little is found in the surrounding atmosphere. However, DEHP molecules that are present in air will adsorb onto dust particles and will be deposited on surfaces through gravity or precipitation. Releases of DEHP to the air from plastic materials, coatings, and flooring in home and work environments, although small, can therefore lead to higher indoor levels than are found in the outdoor air.
DEHP is highly soluble in lipids and can result in increased potential for human health impacts when exposure occurs via certain medical procedures. Medical exposures to infants are of particular concern because of their low body weight and underdeveloped immune system. Medical procedures that can result in increased DEHP exposure in neonates include cardiac bypass procedures, total parenteral nutrition therapy, infusion of lipophilic drugs using PVC bags and tubing, and respiratory therapy
Human Health Effects
Studies indicate that DEHP is a potential human carcinogen and that it likely impacts developmental and reproductive processes of, in particular, male infants. The oral toxicity of DEHP in humans is limited to gastrointestinal (GI) symptoms (mild abdominal pain and diarrhea).
DEHP is currently classified by the USEPA as a Class B2 (probable human) carcinogen. This determination is based entirely on liver cancer in rats and mice.
In 2000 IARC changed its classification for DEHP from "possibly carcinogenic to humans" to a Class 3 carcinogen, "not classifiable as to its carcinogenicity to humans," because of the differences in how the livers of humans and primates respond to DEHP as compared with the livers of rats and mice.
The California Occupational Health and Human Services classified DEHP as a carcinogen in 1988, and it has remained listed in the California Proposition 65 legislation as such since that time.
Studies in rodents exposed to doses in excess of 100 mg/kg/day of DEHP clearly indicate that the testes are a primary target organ, resulting in decreased testicular weights and tubular atrophy.
Oral exposure to DEHP also appears to negatively impact the seminal vesicles, epididymis, and prostate gland in rats and mice. When DEHP enters the human body, the compound is rapidly metabolized into various substances that are readily excreted.
The primary metabolite created is mono-ethylhexyl phthalate (MEHP), which is thought to be responsible for much of DEHP's reproductive toxicity. A review of various studies indicates that developmental, reproductive and hepatic toxicity in laboratory animal. Because the majority of conversion of DEHP to MEHP occurs in the GI tract, exposures to DEHP by ingestion may be more hazardous than those by the intravenous route, which largely bypass the GI tract.
Based on an evaluation of multiple studies, the US National Toxicology Program (NTP) has determined that exposure of neonates to DEHP is a "serious concern". Specifically, the developing organism is more sensitive to DEHP than the juvenile or adult organism. In addition, the age at first exposure to DEHP appears to have a clear influence on the primary reproductive system effect, testicular damage. As a result of its review of associated studies, the NTP has determined that no adverse effects are observable in males at concentrations below 3.7 mg/kg bw/day.
DEHP has been listed as a developmental toxin under California Proposition 65 since 2003.
DEHP is widespread in the environment. According to EPA, it is often found near industrial settings, landfills, and waste disposal sites.
DEHP is not chemically bound to the polymer matrix and can therefore be released throughout the lifecycle of products. DEHP enters the environment through releases from manufacturing facilities that make or use DEHP and from consumer products that contain it. Over long periods of time, it can also migrate out of plastic materials and into the environment.
When DEHP is released to soil, it usually attaches strongly to the soil and does not move very far away from where it was released. DEHP has also been found in groundwater near waste disposal facilities. When DEHP is released it dissolves very slowly into underground water or surface waters that contact it.
Agency for Toxic Substances and Disease Registry "Toxicological Profile for Di (2-ethylhexyl) phthalate (Update)" 2002; Barnehag et al. "The Association between Asthma and Allergic Symptoms in Children and Phthalates in House Dust: A Nested Case-Control Study" Environmental Health Perspectives 2004; Barnehag et al "Phthalates in Indoor Dust and Their Association with Building Characteristics" Environmental Health Perspectives 2003; Gray and Butterworth "Testicular atrophy produced by phthalate esters" Archives of Toxicology 1980; Lamb et al "Reproductive effects of four phthalic acid esters in the mouse" Toxicology and Applied Pharmacology 1987; National Toxicology Program Center for the Evaluation of Risks to Human Reproduction: Expert Panel Update on the Reproductive and Developmental Toxicity of Di (2-Ethylhexyl) Phthalate 2005; USEPA "Technical Factsheet on: Di (2-ethylhexyl) phthalate (DEHP)" 2005