Academic journal article Environmental Health Perspectives

Urinary Biomarkers for Phthalates Associated with Asthma in Norwegian Children

Academic journal article Environmental Health Perspectives

Urinary Biomarkers for Phthalates Associated with Asthma in Norwegian Children

Article excerpt

Phthalates are widely used as plasticizers in consumer products such as building materials, toys, food packaging, cosmetics, and medical devices (Schettler 2006). The length of the alkyl chains gives rise to different molecular weights and functionality between the different types of phthalates. There is no covalent bond between phthalates and the plastics in which they are mixed, and phthalates are therefore easily released into the environment. Human exposure occurs through ingestion, inhalation, and dermal contact, with contaminated food considered to be the most important source of exposure to highmolecular weight phthalates (high-MWP; metabolites > 250 Da) for the general population (Schettler 2006). The use of personal care products may increase exposure to low-MWP (Just et al. 2010; Silva et al. 2004).

Phthalate metabolite concentrations in urine represent a measure of exposure from multiple sources and routes. The only study that has reported on the phthalate burden in a Norwegian population compared concentrations of phthalate metabolites in pregnant women from Norway, the Netherlands, and the United States and found comparable levels among these three groups of women, with estimated average daily intakes below the recommended maximum intake (Ye et al. 2009). Phthalates have also been found in abundance in indoor air particulate matter in Norwegian dwellings and schools (Rakkestad et al. 2007), but so far no data on the body burden of phthalates in children in Norway are available.

In the last decade, several studies have reported associations between phthalate exposure and asthma and allergic disease (Jaakkola and Knight 2008). The findings differ among the phthalates, but most often the heavier phthalate metabolites have had impact on allergic disease development in animal models (Kimber and Dearman 2010). In in vitro studies, the monoester metabolite of di(2-ethylhexyl) phthalate (DEHP), mono(2-ethyl-hexyl) phthalate (MEHP), induced a release of inflammatory mediators from lung cells, including tumor necrosis factor ? (Rakkestad et al. 2010), a pro-inflammatory cytokine that has been implicated in many aspects of the airway pathology of asthma. Several phthalates, including diisodecyl phthalate (DIDP) and phthalate metabolites such as MEHP, can activate peroxisome proliferator-activated receptors that participate in a range of cellular processes including positive and negative regulation of inflammation (Cho et al. 2008; Lovekamp -Swan and Davis 2003). In epidemiological studies, asthma and allergic diseases in children have been associated with house dust concentrations of several high-MWP that are often used in polyvinyl chloride (PVC) flooring (Bornehag et al. 2004; Kolarik et al. 2008). An early follow-up investigation of children from the same birth cohort evaluated in the present study reported that DEHP was the major phthalate in house dust (Oie et al. 1997) and that bronchial obstruction was associated with phthalate-containing PVC flooring and plastic surface materials at home (Jaakkola et al. 1999). There are few reports on associations between biomarkers of phthalate exposure and respiratory outcomes, although one study reported an inverse association between urinary concentrations of monoethyl phthalate (MEP), a metabolite of diethyl phthalate (DEP), and lung function in adult men (Hoppin et al. 2004).

The aim of the present study was to explore the association between urinary concentrations of phthalate metabolites and current asthma in children.


Design and subjects. The present cross-sectional study includes 10-year-old children from the Environment and Childhood Asthma (ECA) study in Oslo, Norway, which is described in detail elsewhere (Lodrup Carlsen 2002). Briefly, this birth cohort included 3,754 healthy infants born in Oslo during a 15-month period beginning 1 January 1992. The ECA study design involved clinical investigations of two main study populations within the birth cohort. …

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