Humans are exposed to chemicals every day in our indoor environment. Chemicals have contributed to increased prosperity but also caused negative health effects. Children are vulnerable to chemicals because of their development and they breathe and drink more in relation to their body weight. That is why it’s important to reduce chemical exposure in environment for children. Preschools have a central role when it comes to materials and products that may pose a risk for exposure. The municipality has an important role to achieve a nontoxic environment which is based on a Swedish environmental quality goal (Non-toxic environment). This study is a part of the prioritized local environmental work in the municipal of Nordmaling. An inventory has been done to find out what type of chemicals that may expose children to harmful effects in preschools of Nordmaling. Electronic as a toy, soft and smelling toys, plastic around food and drinks, foam play pads were common products found during the inventory. This materials containing phthalates, brominated flame retardants, perfluorinated compounds, bisphenol A, lead and cadmium that can expose children through leaching into the indoor environment. A guidance have been constructed to achieve a non-toxic environment based on the results from the inventory in a cost effective way. The conclusion of the report is clear, identified problem areas can quickly be accomplished with small measures and low costs. Increased awareness of harmful substances and good routines for purchases and cleaning can further reduce the exposure to chemicals in the preschools.

For the past few years there has been increasing concern surrounding a group of chemicals known as phthalate esters. In mammals, phthalates are known antiandrogens, interfering with the production or activity of testosterone. Phthalates are ubiquitous in the aquatic environment. With recent findings suggesting that antiandrogens may be responsible for much of the endocrine disruption found in wild fish populations, the study of phthalate esters has become integral to determining whether or not these anti-androgenic chemicals are of concern. I investigated whether di-n-butyl phthalate (DBP) was able to cause antiandrogenic endocrine disruption in fish under controlled laboratory conditions. Three experiments were undertaken. In the first study, two generations of fathead minnows were exposed to nominal concentrations of 6 to 100 μg/L for 21 and 150 days, respectively. The second experiment examined the effects of early life-stage exposure to DBP (50, 100 and 200 μg DBP/L) on three-spined sticklebacks. The final experiment examined the effects of DBP on adult male three-spined sticklebacks in a 21-day nesting study (15 and 35 μg DBP/L). DBP had no effect on the fecundity, survival, growth, sex ratio, or gonadal histology of the exposed fish in any of the experiments. Further, it failed to alter the expression of two steroidogenic genes in adult male sticklebacks. In contrast, DBP was often found to significantly alter plasma androgen concentrations in both species, and spiggin concentrations in the three-spined stickleback, most notably causing significantly reduced spiggin concentrations in the adult males exposed to DBP. Ultimately, DBP-exposure did not disrupt the ability of the fish to reproduce successfully, and did not appear to alter reproductive behaviours or the expression of secondary sexual characteristics. In conclusion, while DBP did appear to have some capacity for endocrine disruption in fish, it was unable to interfere with the ability of the fish to develop normally and reproduce successfully. Thus, environmentallyrelevant concentrations of phthalate esters are likely not of particular concern to fish populations.

Children are constantly exposed to many chemicals via the products they come in contactwith in their everyday life. One chemical group is phthalates, the most commonly usedplasticisers in the world. Phthalates are used mainly in PVC plastic products like floors, toys,food containers and wallpaper but they are also used in rubber, glue, paint, cables etc. Sincethese chemicals are weakly chemically bound to the PVC they can leak and migrate to the air,food, water and skin. Children are exposed to phthalates mainly through food, but because ofthe hand to mouth behaviour they are also exposed via dust inhalation and dust ingestion.About ten years ago regulations of the most toxic phthalates in toys and child care productswere implemented in the EU and from February 2015 it is a general prohibition for the use ofDEHP (diethylhexyl phthalate), DnBP (di-n-butyl phthalate), DiBP (diisobutyl phthalate) andBBzP (butyl benzyl phthalate). DiNP (diisononyl phthalate) is a relatively new phthalate andit has replaced DEHP to some extent in floors and toys. In phthalate free products DINCH(1,2-cyclohexane dicarboxylic acid diisononyl ester) is one of the plasticizer replacingphthalates. The banned phthalates have been shown to cause adverse effects on reproductionand recent research also investigates links between phthalate exposure and asthma and allergysymptoms in children. More experimental animal studies are needed to further investigate theasthma and allergy correlation. In the present project dust samples were collected from 30 preschool indoor environments inthe Stockholm city area to evaluate the levels of the six substances mentioned and thephthalate DEP (diethyl phthalate). The main aim of this thesis project was to search forrelations and links between the phthalate concentrations in dust and parameters from theindoor environment in preschools. Studied parameters are e.g. construction year, floor type,cleaning routines and quantity of toys and furniture made of plastic or foam. The project wascommissioned by the Swedish EPA and performed at the Institute of Environmental Medicine(IMM) at Karolinska Institutet. A negative relation was found between dust phthalate (DEHP and DnBP) concentrationand construction year. Also rooms with old PVC floors had higher concentrations of DEHPand DnBP in dust than rooms with new PVC floors. There was also a trend that dust frompreschools with PVC floors had higher DiNP concentration than dust from preschools withother floor types. The preschools that used foam mattresses for resting had higher DiNPconcentrations than those with no foam mattresses. Most preschools had new foammattresses, which could indicate a more common use of DiNP in new mattresses or mattress2covers compared to old mattresses that contains more DEHP. The four Waldorf preschoolsthat participated had lower DiNP dust concentrations than the other preschools, which wasexpected since Waldorf orientation includes using as little plastic material as possible. Norelation was found between the phthalate dust concentrations and the quantity of toys made ofsoft plastic in the sampled area. Many preschools had made a plastic inventory where they removed old and soft plastic toysand material. Also many preschools recently replaced old foam mattresses used for resting.This could be due to the big chemical focus in the media and authorities and the brochuresthat have been sent out the last couple of years about what preschool can do to decrease thechemical exposure of children. This interest and awareness seen in the preschools waspositive and hopefully the trend spreads to more preschools. Since children spend a big part oftheir time at preschools it is an important mission for society and the government to decreasethe exposure to hazardous chemicals there. Hopefully what has been done so far is just thebeginning.

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Due to the widespread use of the endocrine disruptors Bisphenol-A (BPA) and phthalates in many plastic consumer goods, medical equipment, and personal care products, more than 95% of the US population show detectable levels of urinary BPA and phthalate metabolites. Both have been linked to increased body mass index (BMI in kg/m2), an inexpensive diagnostic tool for obesity, which may however not reflect body fatness. Since excess body fat is associated with cardiovascular diseases, cancer and type II diabetes, it is important to understand the relationship between body fat composition and exposure to BPA and phthalates, a relationship that is still unknown. Using NHANES 1999-2006 data on adults aged >20 years, we investigated the relationship between urinary BPA (N=2,534), monoethyl-phthalate (mEP, N=5,431), monobutyl-phthalate (mBP), monoethylhexyl-phthalate (mEHP) and monobenzyl-phthalate (mBzP, each N=5,436) measured by high-performance liquid chromatography tandem mass spectrometry, and body fat composition measured as lean mass (LM, grams), fat mass (FM, grams) and percent body fat (%BF) using Dual Energy X-ray Absorptiometry. A multivariable linear regression analysis yielded that independently of BMI, BPA, mBP, and mBzP were inversely associated with LM (quartile 4 b=-862.16 (354.65), -731.76 (248.89), -909.13 (252.32), respectively; all p<0.02, p-trend<0.02); mEHP and FM were inversely associated (quartile 4 b=-297.98 (144.87), p=0.04, p-trend<0.02); BPA, mBP, and mBzP were positively associated with %BF but not clinically significant. These results provide novel insights in the relationship between urinary BPA, phthalates and LM independent of BMI, and it highlights the need for prospective studies establishing temporality of this relationship.

Phthalates, chemicals found in a variety of consumer goods and personal care products, may adversely affect fetal neurodevelopment. Women are exposed to a mixture of phthalates during pregnancy because of the common presence of these chemicals in consumer goods. The aim of this study is to investigate potential associations between phthalate exposure during the first trimester of gestation and Intelligence Quotient (IQ) scores of 3-year old children.

Phthalates are industrial chemicals added to plastics found in products such as children’s toys, cosmetics, and household items, and some laboratory studies suggest phthalates may increase levels of inflammation. Chronic inflammation is associated with many chronic health conditions, such as diabetes and rheumatoid arthritis. Although research is limited, recent studies suggest a strong positive relationship between mono-butyl phthalate (MBP), mono-isobutyl phthalate (MiBP), and monocarboxynonyl phthalate (MCNP) and c-reactive protein (CRP), as well as monoethyl phthalate (MEP) and mono-3-carboxypropyl phthalate (MCPP) and interleukin-6 (IL-6). Additionally, this relationship has not been examined among postmenopausal women, a population that is at higher risk of developing chronic health conditions. Our aim was to examine the association between urinary phthalate biomarkers and inflammation biomarkers among postmenopausal women using baseline data from a subset of participants of the Women’s Health Initiative (WHI) (n=443). Phthalate exposure was assessed using phthalate biomarkers (i.e. phthalate metabolites or their molar sum) from urine samples collected at WHI clinical centers from 1993-1998. We measured 13 phthalate metabolites: MEP, MBP, mono-hydroxybutyl phthalate (MHBP), MiBP, mono-hydroxyisobutyl phthalate (MHiBP), monobenzyl phthalate (MBzP), MCPP, mono (2-ethylhexyl) phthalate (MEHP), mono (2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono (2-ethyl-5-oxohexyl) phthalate (MEOHP), mono (2-ethyl-5-carboxypentyl) phthalate (MECPP), mono-carboxyoctyl phthalate (MCOP), and MCNP. Serum and plasma inflammatory biomarker levels (i.e. CRP, IL-6) were measured in separate WHI ancillary studies, using blood samples collected at baseline. We used multivariable linear regression to analyze associations between each phthalate biomarker and inflammation biomarker, adjusting for important covariates. Phthalate biomarkers MCNP (Model 1: b = 0.523; Model 2: b = 0.362) and MCOP (Model 1: b = 0.384; Model 2: b = 0.240) were positively associated with CRP. Additionally, MCNP (Model 1: b = 0.369; Model 2: b = 0.181) was positively associated with IL-6. Statistically significant associations were not observed among the remaining phthalate biomarkers. Our findings suggest that certain phthalates may be related to increasing levels of inflammation.

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Phthalates have been used pervasively as plasticizers in consumer products and building materials. These semi-volatile organic compounds (SVOCs) are ubiquitous in indoor environments, redistributing from their original sources to indoor air, and subsequently to all interior surfaces. Because they partition strongly to surfaces, most phthalates persist for years after the source is removed. Biomonitoring data based on blood and urine testing provide direct evidence of the universal and significant human exposure to phthalates, which may result in serious adverse health effects. However, effective strategies to limit exposures to phthalates remain hamstrung by our poor understanding of their sources and fate and transport in indoor environments. The goal of this research is to explicitly elucidate the fundamental mechanisms governing emission, transport, and human exposure associated with phthalates in indoor environments. The specific research objectives are to 1) develop a novel, rapid, small-chamber method to determine the key parameters that control phthalate emissions and characterize the emissions; 2) investigate the influences of temperature, air flow rate, and surface sorption on phthalate emissions via a series of controlled tests in small and large chambers; 3) develop and validate a new indoor fate and transport model for phthalates with consideration of particle dynamics and its effects on emission and sorption. This research, which connects emission measurements to chemical transport and exposure assessment, will explicitly elucidate the fundamental mechanisms governing emission, transport, and human exposure associated with phthalates in indoor environments. / text

Phthalates are industrial plasticizers with a wide range of applications. Di-(2-ethylhexyl) phthalate (DEHP) is one of the most highly produced and frequently studied phthalates. Its metabolite, mono-(2-ethylhexyl) phthalate (MEHP) is known as a testicular toxicant. The objective of this study was to examine expression of the genes of interest in testicular germ cells exposed to MEHP in a dose- and time-dependent manner at concentrations of 1µM, 10µM, and 100µM at 24, 48, 72 and 96hr time points. The genes consisted of Testisin, GSPT1, and MGMT genes which are a tumor suppressors, phase II xenobiotic metabolizing enzyme and DNA repair gene respectively. These genes were analyzed by Quantitative Real Time PCR (RT-PCR). The results revealed an overall down-regulation for each gene as the concentration and/or time increased. Testisin was the focus of the gene expression analysis. Testisin is epigenetically silenced in testicular germ cell tumors (TGCT) by DNA methylation at the 5’CpG island of the gene. To investigate if MEHP is capable of DNA hypermethylation, a co-exposure with 5-azacytidine (demethylating agent) was conducted. Compared with the 5-azacytidine treatment alone, there was a significant down-regulation of the Testisin gene in the co-exposure. This suggests that MEHP may down-regulate Testisin gene expression by DNA methylation. These findings provide evidence that MEHP can alter the expression of Testisin, GSTP1 and MGMT, genes that are associated in the risk of developing testicular germ cell tumors. In addition, results indicated that MEHP may cause DNA methylation leading to the down-regulation/silencing of genes such as Testisin.