ENDOCRINE DISRUPTOR CHEMICALS - Plastics and Environmental Sustainability - page 297

et al., 2007). This is hardly a surprise as the available data suggests life-long
human exposure to occur from in utero through death of individuals.

Table 7.6 Typical Concentrations of DEHP in Water and Air
Source: Adapted from Clark et al. (2003).
Medium Units Mean concentration Median and range
Drinking water µg/l 0.55 0.55 (0.16-170)

Wastewater µg/l 27 8.3 (0.01-4400)

Rainwater µg/l 0.17 0.17 (0.004-0.68)

Surface water µg/l 0.21 0.05 (<0.002-137)

ng/m 3 5.0 Outdoor air 2.3 (<0.4-65)

ng/m 3 109 Indoor air 55 (20-240)

The relatively low human body load of phthalates is a result of short
residence times (elimination half-life 8-10 h) in the body as phthalates are
not bioaccumulative. 9 Better quantification of exposure might be achieved
via the monitoring of primary metabolite from hydrolysis of the phthalate
(Kamrin, 2009).

The chronic oral reference dose of 0.02 mg/kg/day of DEHP derived by
the USEPA is based on the lowest observable doses in experimental studies
carried out several decades ago. As with BPA, at the time, studies on
low-dose health effects of phthalates were not available. Phthalate levels in
Table 7.6 are well below the oral reference level but in common with all
EDCs may have low-level effects.

7.3.1 Exposure to Phthalates

The primary route of exposure to phthalates is via ingestion (Wormuth et
al., 2006), while inhalation (Huang et al., 2011) and dermal contact (Koo
and Lee, 2005; Rudel et al., 2003) may also play a role. Phthalates in food
packaging leached into food is the primary source of ingested phthalates.
High levels of DBP (5860 mg/kg) and DEHP (3680 mg/kg) in food
packaging have been reported (Versar, Inc. and Syracuse Research
Corporation, 2010). Partitioning of phthalates into food is particularly high
with products such as cheese, butter, oils, and milk. Versar, Inc. and
Syracuse Research Corporation (2010) summarized the highest reported