“…The ADDs of PAEs for children and adults through dust ingestion were 1.46–1.56 orders higher than that of dust inhalation and dermal adsorption. Similar results have been reported and documented by other researchers and reviewers 12 , 76 , 78 – 80 .…”
Section: Resultssupporting
confidence: 92%
“…The highest contributions of D n OP and DEP could be linked with plasticizers and personal care products containing D n OP and DEP in the indoor environment 10 , 67 . In addition, the result of a chamber study on the migration of D n OP between source surfaces and settled dust by Li et al 78 is a pointer to the fact that direct contact contributes significantly to the migration of D n OP from the sources to the dust. Figure 3 Composition profiles of PAEs in indoor dust.…”
The levels, profiles of Phthalate acid esters (PAEs) and their associated health risk in children and adults using indoor dust samples were assessed from nine (9) microenvironments in Nigeria. Six PAEs congeners were determined using Gas Chromatography–Mass Spectrometry and the human health risk assessments of PAEs exposure to children and adults were computed using the United States Environmental Protection Agency (USEPA) exposure model. The mean concentrations of the total PAEs (Σ6PAEs) in indoor dust across the study locations ranged from 1.61 ± 0.12 to 53.3 ± 5.27 μg/g with 72.0% of di-n-octyl phthalate (DnOP) as the most predominant contributor of PAEs in sample locations B, C, D, E, F and G. PAEs estimated daily intake results exceeded the USEPA value of 20 and 50 kg/bw/day for children and adults respectively in some locations. Non-carcinogenic risk exposure indicated no risk (HI < 1), while the carcinogenic risk was within the recommended threshold of 1.00 × 10–4 to 1.00 × 10–6 for benzyl butyl phthalate and bis-2-ethylhexyl phthalate. From our findings, lower levels of PAEs were observed in locations with good ventilation system. Also, the human health risk evaluation indicated indoor dust ingestion as the dominant exposure route of PAEs for both children and adults, while the children were at a higher risk of PAEs exposure. To protect children susceptible to these endocrine-disrupting pollutants, soft vinyl children’s toys and teething rings should be avoided. Appropriate policies and procedures on the reduction of PAEs exposure to humans should be enacted by all stakeholders, including government regulatory agencies, industries, school administrators and the entire community.
“…The ADDs of PAEs for children and adults through dust ingestion were 1.46–1.56 orders higher than that of dust inhalation and dermal adsorption. Similar results have been reported and documented by other researchers and reviewers 12 , 76 , 78 – 80 .…”
Section: Resultssupporting
confidence: 92%
“…The highest contributions of D n OP and DEP could be linked with plasticizers and personal care products containing D n OP and DEP in the indoor environment 10 , 67 . In addition, the result of a chamber study on the migration of D n OP between source surfaces and settled dust by Li et al 78 is a pointer to the fact that direct contact contributes significantly to the migration of D n OP from the sources to the dust. Figure 3 Composition profiles of PAEs in indoor dust.…”
The levels, profiles of Phthalate acid esters (PAEs) and their associated health risk in children and adults using indoor dust samples were assessed from nine (9) microenvironments in Nigeria. Six PAEs congeners were determined using Gas Chromatography–Mass Spectrometry and the human health risk assessments of PAEs exposure to children and adults were computed using the United States Environmental Protection Agency (USEPA) exposure model. The mean concentrations of the total PAEs (Σ6PAEs) in indoor dust across the study locations ranged from 1.61 ± 0.12 to 53.3 ± 5.27 μg/g with 72.0% of di-n-octyl phthalate (DnOP) as the most predominant contributor of PAEs in sample locations B, C, D, E, F and G. PAEs estimated daily intake results exceeded the USEPA value of 20 and 50 kg/bw/day for children and adults respectively in some locations. Non-carcinogenic risk exposure indicated no risk (HI < 1), while the carcinogenic risk was within the recommended threshold of 1.00 × 10–4 to 1.00 × 10–6 for benzyl butyl phthalate and bis-2-ethylhexyl phthalate. From our findings, lower levels of PAEs were observed in locations with good ventilation system. Also, the human health risk evaluation indicated indoor dust ingestion as the dominant exposure route of PAEs for both children and adults, while the children were at a higher risk of PAEs exposure. To protect children susceptible to these endocrine-disrupting pollutants, soft vinyl children’s toys and teething rings should be avoided. Appropriate policies and procedures on the reduction of PAEs exposure to humans should be enacted by all stakeholders, including government regulatory agencies, industries, school administrators and the entire community.
“…Given that off-gassing of HMW phthalate from the vinyl floor generally occurs during first few weeks to months after installation, depending on other factors such as temperature and ventilation [50], information on when the vinyl floor is introduced is useful to understand the mechanism. Further, we speculate that due to the transfer of DEHP from the floor material to dust [16,51,52], the DEHP concentration in dust in the kitchen and bathroom of houses with vinyl floors may have been greater, and hence infants spending more time in those rooms could have experienced even higher exposures. Broadly, these observations indicate that avoiding vinyl floors in selected rooms (e.g., bedrooms) may not be sufficient in reducing DEHP exposure at home.…”
Section: Associations Between Dehp and Housing Characteristicsmentioning
Background. Di-(2-ethylhexyl) phthalate (DEHP), which is ubiquitous in indoor environments, was the predominant phthalate measured in house dust in the Canadian CHILD Cohort and was found to be associated with a large increased risk of childhood asthma. Objective. To inform interventions by identifying sources of DEHP in dust and assessing behaviors related to DEHP concentrations in house dust. Methods. DEHP levels were measured in 726 dust samples collected at ~3 months of age in CHILD as well as in ~50 homes at two time points (June and November) in the CHILD pilot study. DEHP metabolites were measured in urine for a subset of the ~3-month-old infants. Housing characteristics were assessed at the time of dust and urine collection. Numerous factors from these surveys were investigated as potential sources of DEHP using univariate analyses and multivariable regressions. Correlations between DEHP in dust and urinary metabolites and between repeat dust samples were examined to study the relationship between dust measurement and DEHP exposure. Results. Overall, DEHP dust concentrations were higher for lower-income families. Homes with vinyl flooring in the kitchen and bathroom showed higher levels of DEHP than those without vinyl flooring. The quantity of vinyl furniture and the presence of mold were associated with higher DEHP concentrations, while the use of mattress covers reduced concentration. No other significant associations were found. DEHP concentrations in dust were consistent over 6 months, although the correlation between dust and DEHP metabolites in urine was low. Conclusion. DEHP in house dust persisted over multiple months, contributed to infant internal exposure, and was associated with specific housing characteristics. These findings may inform the public on their choice of building materials and products, as well as future policies, aimed at reducing the health risk associated with exposures in the indoor environment especially for children.
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