Exposure to Organophosphate Ester (OPE) Flame Retardants & Plasticizers

Why is exposure to OPE relevant to health?

Several classes of flame retardants are used in consumer products. As legacy brominated flame retardants (BFR) are phased-out due to concerns about their bioaccumulation and toxicity, they are increasingly being replaced with OPE flame retardants. OPE are added to a wide variety of products, including plastics, polyurethane foam, textiles, furniture, and electronics, to reduce their flammability and to meet state, federal, and international flammability standards. Some organophosphate triesters are also used as plasticizers in building materials and cosmetics such as nail polishes.

Studies have reported widespread exposure of humans to OPE (Hoffman et al., 2017, 20174a; Kim and Kannan, 2018; Wang et al., 2019). OPE have been reported to occur in a wide range of consumer products, indoor air, water, and foodstuffs. In environmental samples, OPE are expected to be present predominantly as parent trimester compounds, whereas that in biological specimens such as urine, diesters are more prevalent (Wang et al., 2019). For example, two commonly used OPE triesters, tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) and triphenyl phosphate (TPHP) are hydrolyzed to bis(1,3-dichloro-2-propyl) phosphate (BDCIPP) and diphenyl phosphate (DPHP), the metabolites of TDCIPP and TPHP, respectively, in the human bodies. Toxicological studies have linked exposure to OPE with reproductive and developmental effects (Behl et al., 2015), and genotoxicity and endocrine effects (Chen et al., 2015). Although exposure to some of these newer flame retardants may be widespread, potential health effects related to these exposures are not well understood.

What types of questions can be answered?

Following exposure, OPE such as TPHP and TDCIPP are hydrolyzed in the human body to yield diester metabolites, which are excreted in urine (Cequier et al., 2015). Therefore, urinary OPE metabolites have been used as biomarkers of OPE exposure (Dodson et al., 2015; Hoffman et al., 2014b). Exposure to OPE in humans can be estimated by measuring their diester metabolites in urine. The sources and pathways of human exposure can be assessed by measurement of parent triesters in indoor air, hand wipes, household dust, and wristbands.

How can exposure to OPE be measured?

  • Analytes: Exposure to OPE can be measured by quantifying their metabolites in urine, or parent compounds in environmental samples, such as indoor air, hand wipes, house dust or wristbands.
  • Methods: Most OPE metabolites and parent compounds are quantified use liquid chromatography coupled with tandem mass spectrometry.
  • Types of biospecimens: Urine is the most commonly used biological matrices for OPEs.
  • Types of environmental samples: Air, hand wipes, and wristbands are the most common media analyzed.

How does HHEAR ensure the quality of its analyses?

If possible, the inclusion of field “blanks” in a study can help identify any contamination from collection/storage sources. All assays are validated with respect to accuracy and precision. Quality control samples are included in each batch of analysis. Laboratories participate in proficiency testing programs to validate assays.

What sample quality and quantity are necessary?

This is highly dependent on the assay to be run and the sample type, but in general a few milliliters of urine or 500 milligrams of dust are required. Less volume/mass usually translates to lower frequency of detection. Multiple freeze-thaw cycles should not be a significant problem for the analysis of these substances.


Behl M, Hsieh JH, Shafer TJ, et al. Use of alternative assays to identify and prioritize organophosphorus flame retardants for potential developmental and neurotoxicity. Neurotoxicol. Teratol. 2015;52:181-193.

Cequier E, Sakhi AK, Marce RM, et al. Human exposure pathways to organophosphate triesters - a biomonitoring study of mother-child pairs. Environ. Int. 2015;75:159-165.

Chen G, Zhang S, Jin Y, et al. TPP and TCEP induce oxidative stress and alter steroidogenesis in TM3 leydig cells. Reprod. Toxicol. 2015;57:100-110.

Dodson RE, Van den Eede N, Covaci A, et al. Urinary biomonitoring of phosphate flame retardants: Levels in California adults and recommendations for future studies. Environ. Sci. Technol. 2015;48:13625-13633.

Hoffman K, Butt CM, Webster TF, et al. Temporal Trends in Exposure to Organophosphate Flame Retardants in the United States. Environmental Science and Technology Letters. 2017;4:112-118.

Hoffman K, Gearhart-Serna L, Lorber M, et al. Estimated Tris(1,3-dichloro-2-propyl) Phosphate Exposure Levels for U.S. Infants Suggest Potential Health Risks. Environmental Science and Technology Letters. 2014a;4:334-338.

Hoffman K, Daniels JL, Stapleton HM. Urinary metabolites of organophosphate flame retardants and their variability in pregnant women. Environ. Int. 2014b;63:169-172.

Kim U, Kannan K. Occurrence and Distribution of Organophosphate Flame Retardants/Plasticizers in Surface Waters, Tap Water, and Rainwater: Implications for human exposure. Environmental Science and Technology. 2018;52:5625-5633.

Wang Y, Li W, Martínez-Moral M-P, et al. Metabolites of organophosphate esters in urine from the United States: Concentrations, temporal variability, and exposure assessment. Environment International. 2019;122:213-221.