This study investigated the influence of three indoor environmental parameters: ventilation (expressed as air exchange rate, h-1), temperature, and relative humidity, on phthalate concentration in dust and in estimated airborne. We monitored environmental parameters and collected dust samples in 327 bedrooms in Tianjin, China. Air exchange rates were estimated using occupants-generated CO2 as a tracer gas. Six common phthalates were analyzed as components of dust: Diethyl Phthalate (DEP), Di-isobutyl Phthalate (DiBP), Di-n-Butyl Phthalate (DnBP), Benzyl Butyl Phthalate (BBzP), Di (2-Ethylhexyl) Phthalate (DEHP) and Di-isononyl Phthalate (DiNP). Phthalate concentrations were compared among environmental parameters categorized as low (below median) and high (above median) using Mann-Whitney U tests. Quantitative associations of phthalate concentrations with environmental parameters were further explored with exponential fittings based on a binning method. We observed a dilution effect of ventilation on low molecular weight phthalates, which was significant for DiBP, whose concentration decreased by 32 % with an increase in air exchange rate (Delta = 1 h-1). We found a positive association between phthalate concentrations and indoor air temperature; the dust-phase phthalate concentration increased by 11 %, for each 1 degrees C increase in indoor air temperature. The results indicate that continuous ventilation may be an effective strategy to reduce concentrations of the more volatile phthalates in homes. A higher indoor temperature may lead to increased phthalate concentrations in home environments.

Phthalates are common in polyvinyl chloride (PVC) plastics and numerous consumer goods in our homes from which they can migrate and adhere to indoor dust particles. It is known that indoor dust exposure contribute to human phthalate intake; however, there is a lack of large studies with a repeated-measure design investigating how phthalate levels in indoor dust may vary over time in people's homes.

This study investigated levels of seven phthalates and one alternative plasticiser di-iso-nonyl-cyclohexane-di-carboxylate (DiNCH) in bedroom dust collected prenatally around week 25 during pregnancy and postnatally at six months after birth, from 496 Swedish homes. Prenatal and postnatal phthalate levels were compared using correlation and season-adjusted general linear regression models.

Over the nine-month period, levels of six out of seven phthalates were associated as indicated by a positive Pearson correlation (0.18 < r < 0.50, P < .001) and Lin's concordance correlation between matched prenatal and postnatal dust samples. Compared to prenatal levels, the season-adjusted postnatal levels decreased for five phthalates, whilst di-ethyl-hexyl phthalate (DEHP), di-2-propylheptyl phthalate (DPHP) and DiNCH increased.

The results suggest that families with higher phthalate levels in bedroom dust during pregnancy are likely to remain among those with higher levels in the infancy period. However, all average phthalate levels changed over this specific nine-month period suggesting that available phthalate sources or their use were altered between the dust collections. Changes in home characteristics, family lifestyle, and phthalate replacement trends may contribute to explain the differences.

Background Prenatal maternal phthalate exposure has been associated with wheeze and asthma in children, but results are inconclusive. Previous studies typically assessed exposure in late pregnancy, included only a small number of old phthalates, and assessed outcomes in children aged 5 years or older. Objective We explored associations between 1st trimester prenatal maternal exposure to a wider range of phthalates and wheeze in early childhood. Methods First trimester concentrations of 14 metabolites from 8 phthalates and one alternative plasticizer were quantified in first-morning void urine from 1148 mothers in the Swedish SELMA study. Associations between log-transformed metabolite concentrations and parental reported ever wheeze among 24-month-old children were investigated with logistic regression models adjusted for parental asthma/rhinitis, sex of child, maternal education, smoking, and creatinine. Results Metabolites of replacement phthalates di-iso-decyl phthalate (DiDP) and di-2-propylheptyl phthalate (DPHP) were associated with increased risk for wheeze (aOR 1.47, 95% CI 1.08-2.01 and aOR 1.49, 95% CI 1.04-2.15, respectively). The associations with DiDP and DPHP were stronger among children whose parents did not have asthma or rhinitis. In this group, wheeze was also associated with metabolites of butyl-benzyl phthalate (BBzP) and di-iso-nonyl phthalate (DiNP). Significance Maternal phthalate exposure during early pregnancy may be a risk factor for wheeze in early childhood, especially among children whose parents do not have asthma or rhinitis symptoms.

There is an increasing concern for health risks from exposure to chemical emissions in indoor environments where we spend a lot of time. A chain of complex relationships connects emission sources, exposure, and health effects. For some indoor contaminants, we know a lot about the separate relationships. However, linking specific sources and environmental exposure pathways to hazardous effects is challenging, with a lack of evidence that is needed for risk assessment as a result. This chapter presents the full chain model that follows chemicals and maps the relationships from sources to potential health effects. It is a tool to establish relevant scientific knowledge regarding chemical exposure. The model consists of three overlapping sections: environmental exposure, human exposure, and health effects, and includes relationships between emission sources, environmental pathways, human uptake, and effects on health and development. As a demonstration, results from the Swedish Environmental Longitudinal Mother and child Asthma and allergy (SELMA) study were applied to the full chain model. Phthalates, a group of abundant indoor contaminants, and airway disorders were used as an example. Starting with polyvinyl chloride (PVC) flooring as an emission source, connections were made between indoor dust levels, exposure and uptake among pregnant women, and airway symptoms in young children. By using the full chain model, not only separate relationships were identified. Butylbenzyl phthalate could be followed from a source to elevated environmental exposure and human uptake to associations with a higher risk for airway outcomes in children. 

Phthalates are widely used in consumer products. Exposure to phthalates can lead to adverse health effects in humans, with early-life exposure being of particular concern. Phthalate exposure occurs mainly through ingestion, inhalation, and dermal absorption. However, our understanding of the relative importance of different exposure routes is incomplete. This study estimated the intake of five phthalates from the residential indoor environment for 455 Swedish pregnant women in the SELMA study using phthalate mass fraction in indoor dust and compares these to total daily phthalate intakes back-calculated from phthalate metabolite concentrations in the women's urine. Steady-state models were used to estimate indoor air phthalate concentrations from dust measurements. Intakes from residential dust and air made meaningful contributions to total daily intakes of more volatile di-ethyl phthalate (DEP), di-n-butyl phthalate (DnBP), and di-iso-butyl phthalate (DiBP) (11% of total DEP intake and 28% of total DnBP and DiBP intake combined). Dermal absorption from air was the dominant pathway contributing to the indoor environmental exposure. Residential exposure to less volatile phthalates made minor contributions to total intake. These results suggest that reducing the presence of low molecular weight phthalates in the residential indoor environment can meaningfully reduce phthalate intake among pregnant women.

Phthalates are ubiquitous indoor pollutants which have been associated with child airway disease although results are inconclusive. This study examined associations between phthalate levels in residential indoor dust and croup during infancy. Settled indoor dust was collected in 482 homes of 6-month-old infants in the Swedish Environmental Longitudinal, Mother and child, Asthma and allergy (SELMA) study and analysed for seven phthalates and one phthalate replacement using gas chromatography tandem mass spectrometry. The incidence of parental reported croup at 12 months was 6.4% for girls and 13.4% for boys. Associations between phthalate dust levels and croup were analysed by logistic regression adjusted for potential confounders. We found significant associations between di-ethyl phthalate (DEP) and di-ethyl-hexyl phthalate (DEHP) in residential dust and parental reported croup (adjusted odds ratio (aOR) = 1.71; 95% CI: 1.08-2.73 and 2.07; 1.00-4.30, respectively). Stratified results for boys showed significant associations between DEP and butyl-benzyl phthalate (BBzP) in dust and infant croup (aOR = 1.86; 95% CI: 1.04-3.34 and 2.02; 1.04-3.90, respectively). Results for girls had questionable statistical power due to few cases. Our results suggest that exposure to phthalates in dust is a risk factor for airway inflammatory responses in infant children.

Phthalates are widely used in a large number of consumer goods and building materials from which they can leach and contaminate the environment such as indoor dust and air. It is unclear how phthalate sources in our homes and indoor dust contribute to human intake and airway symptoms in children. 

This thesis aims to contribute to the understanding of phthalate exposure by exploring connections between phthalate sources in home environments, indoor exposure, human intake, and childrens’ airway symptoms. It utilizes data in the Swedish SELMA study, including measurements of indoor dust phthalate levels and corresponding metabolites in prenatal maternal urine, and information on health outcomes and cofactors from self-administered questionnaires. 

The results show higher levels of three phthalates (DnBP, BBzP and DEHP) in dust from homes with PVC flooring. Four phthalates in dust (DEP, DnBP, DiBP, and BBzP) were positively correlated with corresponding maternal urinary metabolites. The dust was estimated to explain a 1-28% (median) contribution to the total daily intake of the analysed phthalates among pregnant women. Living in homes with PVC flooring was linked to a higher intake of BBzP and DEHP. Further, associations were found between prenatal phthalate exposure (BBzP, DiNP, DiDP and DPHP) and wheeze, and phthalates in dust (DEP, BBzP and DEHP) and croup in children before 2-years-of-age.

This thesis connects a full chain of factors relevant for human phthalate exposure. Sources in our homes were linked to higher levels in dust and to human intake. Also, both regulated and non-regulated phthalates were associated with human intake and airway symptoms. Combined with other research results, this implies that using new phthalates as replacements might not be optimal, and we could consider regulating phthalates as a group. Any links to effects in older children is unknown, still, limiting indoor phthalate sources could reduce intake and benefit overall public health.

The indoor environment is important for our health; still, a mix of phthalates, that are either non-regulated or classed as hazardous, can be detected in dust in our homes. The phthalates have leached from various products and building materials such as plastics, electronics, perfume, and interiors. Should this make us concerned?

This thesis has followed indoor phthalate exposure from vinyl (PVC) flooring materials to dust, to phthalate intake among pregnant women, and finally to investigated if airway symptoms in young children are linked to either phthalate exposure of the fetus or phthalates in bedroom dust.

The results show that phthalates from vinyl floorings can be followed through this full exposure chain. Both regulated and non-regulated replacement phthalates were associated with human intake and airway symptoms in children. Combined with other research results, this implies that using new phthalates as replacements might not be optimal, and we could consider regulating phthalates as a group. Although the risk is relatively low for the individual, reducing phthalate sources and exposure during early human development may have benefits on a public health level and contribute to more sustainable use of resources.