The authors analyzed data from a national sample to examine the relationships between blood concentrations of selected volatile organic compounds (VOCs) and the assessment scores of neurobehavioral evaluation tests. They calculated summary statistics to describe blood concentrations of 30 VOCs. For instance, the 95th percentiles were as follows: 1, 1, 1-trichloroethane, 0.799 μg/l; 1, 4-dichlorobenzene, 11.081 μg/l; benzene, 0.476 μg/l; and toluene, 0.281 μg/l. For 1, 4-dichlorobenzene, benzene, dibromochloromethane, and trichloroethene, a blood level higher than the 95th percentile was associated with a poorer neurobehavioral assessment score than was a blood level up to the 95th percentile. The authors found a linear relationship between blood toluene concentration and the Serial Digit Learning Test score. The findings suggest that exposure to certain VOCs may result in poor neurobehavioral performance. The study was exploratory and precludes a conclusive statement, so further investigation is warranted.

No description available.

INTRODUCTION: Chemical exposures to US pregnant women have been shown to have adverse health impacts on both mother and fetus. A prior paper revealed that US pregnant women in 2003-2004 had widespread exposure to multiple chemicals. The goal of this research is to examine how environmental chemical exposures to US pregnant women have changed from 2003 to 2010 and to look further at the extent of simultaneous exposure to multiple chemicals in US pregnant women using biomonitoring data available through NHANES (the National Health and Nutritional Examination Survey). METHODS: Using available NHANES data from the following cycles (2003-2004, 2005-2006, 2007-2008, 2009-2010), we analyzed how environmental chemical exposures changed over time. Covariates were used and data was weighted to reflect the population of pregnant US women. Each cycle was then compared to the 2003-2004 cycle in order to assess how exposures have changed over time. We then looked at the data in an entirely different fashion. We examined the total number of chemicals detected in a given pregnant woman by chemical group. Finally, we looked at the total number of detects across various chemical groups and used the Fisher Exact Test to study how the distribution of detections changed in 2009-2010 compared to 2003-2004. RESULTS: While at least one-third of the chemicals analyzed showed one cycle that differed, exposure rates of individual chemicals were generally not increasing from 2003-2010. Median number of detections over chemical groups also did not show much difference over time. However, analysis of the change in frequency distributions revealed that, for some chemical groups, the frequency of detects in US pregnant woman significantly increased in 2010 compared to 2003. CONCLUSIONS: Widespread chemical exposures were seen in US pregnant women from 2003 through 2010. The number of chemical analytes detected in US pregnant women’s bodies is rising. Many chemicals studied had similar mechanisms of action and/or similar adverse health outcomes upon exposure which is known to result in a cumulative health effect. This research suggests that we need to focus not only on exposure rates of individual chemicals but also on the overall number of chemicals detected when assessing the overall picture of environmental chemical exposures to pregnant women in the US.

Stable isotope analysis (SIA) is a valuable tool in ecotoxicology because δ13C and δ15N may provide insights into the trophic transfer of contaminants in a food web. The relationship between a species’ trophic position (TP, determined from δ15N) and internal concentration of biomagnifying contaminants can be established and used for regulatory purposes. However, the exposure of organisms to xenobiotics incurs physiological costs, and the stable isotope signature of a consumer reflects not only diet but also a physiological state. The latter raises questions regarding the interpretation of stable isotope signatures in contaminated areas. Therefore, the aim of this Thesis was to evaluate the behaviour of consumers’ stable isotope signatures in stressed systems, with a primary focus on the effects of environmental contaminants. In paper I, the physiological costs of chemical exposure were found to alter incorporation rates of dietary nitrogen and carbon in a consumer by influencing both growth and metabolic turnover, with resulting changes in isotope signatures relative to a control system. In paper II, the diet-consumer discrimination factors for 15N and 13C were confirmed to increase under chemical exposure mediated via increased metabolic costs. However, the physiological response was low and translated into only minor shifts in the δ13C and δ15N. The predictability of exposure effects on the stable isotope signature was demonstrated in paper III, in which animals exposed to a chemical with a known mode of action presented expected effects on elemental composition, body size, biomarkers of oxidative stress and the stable isotope signatures. Moreover, consumers’ oxidative balance was found to be related to their δ15N values, thus providing evidence of the kinetic isotope effect on the oxidative status. However, despite the alterations in stable isotope signatures observed in laboratory settings (papers I-III), the effect of xenobiotics on the TP estimates was nil or minor in the field-collected animals. Moreover, the TP values were not significantly different between the animals in the contaminated and the reference habitats because of the high overall uncertainties in the TP estimates (paper IV). Also, the TP estimates based on δ15N in bulk material were more similar between the contaminated and the reference systems than TP estimates based on δ15N values in amino acids. Therefore, the latter method appears more sensitive towards xenobiotics (and, possibly, other environmental stressors) and thus less suitable for TP assessment in contaminated areas. This Thesis improved the overall understanding of the applicability of SIA in stressed systems by establishing relationships between various exposure regimes, physiological responses and the stable isotope signatures in consumers. In model species at low trophic levels, the exposure to xenobiotics was found to significantly affect δ13C and δ15N values, which can be expected whenever physiological responses are detected. However, because of the overall high uncertainty in TP estimates, no significant differences between contaminated and control systems were detected, although the estimated TP were consistently higher in the contaminated systems. Future research should focus on higher trophic levels, in which effects of a greater magnitude can be expected. Moreover, the effects in entire food webs should be addressed rather than single prey–consumer relationships as well as other environmental variables that may contribute to the stable isotope variability in and among systems under various environmental pressures. / <p>At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 3: Manuscript. Paper 4: Manuscript.</p>

No description available.

Background: Environmental exposures acting through different mechanisms have been linked with a number of cancers. Perfluoroalkyl chemicals (PFCs) are endocrine disrupting chemicals affecting estrogen homeostasis. Objectives: We examined the association between PFCs and a group of estrogen related cancers and explored if increased non-occupational exposure was associated with increased odds of developing these cancers. We also explored which of these chemical exposures was more correlated with each cancer. Methods: Using data from the National Health and Nutrition Examination Survey (NHANES), we selected participants ≥ 20 years of age. Our outcome variable was presence or absence of breast, prostate, ovarian and uterine cancer (yes/no); our exposure variables were serum PFCs. Logistic regression models were used in investigating the association between PFCs and cancer types and between quartiles of PFCs exposure concentrations and presence or absence of cancer while adjusting for covariates. Discriminant analysis was used to assess the correlation between individual PFCs compounds and individual cancer types. Results: PFCs were associated with increased odds of ovarian cancer; PFOA: 1.02(1.01, 1.02), PFOS: 1.01 (1.012, 1.013), PFHS 1.031 (1.030, 1.033), PFDE: 1.29(1.27, 1.30) and increased odds of breast cancer; PFOA: 1.089(1.089, 1.09), PFOS: 1.011(1.011, 1.011), PFNA: 1.031(1.030, 1.033), PFHS: 1.02 (1.02, 1.02), PFDE: 1.19(1.18, 1.19). PFCs were not associated with increased odds of prostate or uterine cancers. Comparing the odds in quartile 4 to quartile 1 for ovarian cancer, PFOA: 1.77(1.75,1.79), PFOS: 2.25(2.22, 2.28), PFHS: 1.86(1.84, 1.88), PFDE: 2.11(2.09, 2.14). For breast cancer, PFOA: 2.30(2.28, 2.31), PFOS: 1.47(1.46, 1.48), PFNA: 1.04(1.03, 1.05), PFHS:7.07(6.97,7.17), PFDE: 1.38(1.37, 1.39). PFOA was more correlated with breast cancer (0.7) and PFHS was more correlated with ovarian cancer (0.9). Discussion: PFCs were associated with increased odds of ovarian and breast cancers with a positive dose-response relationship. PFOA was more correlated with breast cancer and PFHS more with ovarian cancer.

No description available.

The human body encounters a number of chemical exposures on a daily basis, which may have short- or long-term health implications. Previously it has been demonstrated that the entire respiratory tract of an individual reacts to exposures like tobacco smoke in a similar manner, and that common molecular changes can be measured in airway epithelium. I propose that cataloguing the exposure of airway epithelial cells to tobacco cigarette (TCIG) smoke and its constituents, electronic cigarette (ECIG) aerosol and other drugs and small molecules can significantly increase the understanding of chemical exposure and identify common gene expression alterations. First, I determined the molecular impact of ECIG aerosol exposure on human airway epithelium in vitro, including alterations in genes related to xenobiotic metabolism, oxidative stress, and ciliated cells. These changes were generally less pronounced than the effects of TCIG exposure, and were more pronounced in ECIG products containing nicotine than those without nicotine. Furthermore, gene expression differences observed in vitro were concordant with differences observed in airway epithelium collected from ECIG users. Second, I examined the impact of TCIG exposure and TCIG constituents on premalignant airway cells, to better understand the progression or regression of precancerous lesions. These data could also identify the constituents of TCIGs and the precancerous mutations that increase the risk for malignancy. Third, in an effort to build a high-throughput methodology for chemical exposures, I exposed primary lung cell lines to small molecule therapeutics and identified lung-specific and lung cell-type-specific effects of exposure, suggesting that profiling additional cell lines would further inform airway gene expression in response to exposure and that organ-specific exposure profiling may provide valuable insight into drug discovery for common diseases. Overall, transcriptomic profiles from the airway epithelium reflect exposure to various inhaled and chemical perturbations. These gene expression profiles indicate common changes across a multitude of airway exposures as well as unique alterations specific to a given perturbation. Gene expression profiling can therefore be used to detail the potential response to a compendium of chemical exposures including those that are either well-established or potential risk factors for chronic lung diseases. / 2019-07-09T00:00:00Z

Asthma and allergies have increased considerably during the past 40-50 years. Along with this increase, a heightened awareness regarding different neuro-developmental disorders such as autism spectrum disorder has occurred and it has been proposed that such disorders are also on the increase. It has been suggested that environmental factors, especially in the indoor environments, may be associated with the increase in these disorder, especially among children, who spend more than 90% of their time indoors. The aim of this thesis has been to investigate certain environmental factors in homes and their impact on children’s health, in terms of asthma, rhinitis, eczema as well as autism spectrum disorders, and to identify certain methodological difficulties in epidemiological investigations. We found that the mean incidence rate per year for doctor diagnosed asthma was in the range of 0.6-2.4% and for incidence of rhinitis 1.1-3.7%. The incidence rate of eczema ever was 2.7%. These results showed that when using a cohort established after birth the estimated incidence rates are strongly dependent of how the baseline population’s health and how the studied health outcome at follow up is defined. Our results showed that the associations between parental reported moisture problems in the home and asthma in children that were revealed in cross-sectional analyses decreased or disappeared when longitudinal data were used on the same data set. Our results therefore indicate that associations between parental reported moisture problems and asthma from cross-sectional questionnaire studies should be interpreted with caution due to the risk for reporting bias. Our results show that children who were living in homes with PVC-flooring in the bedroom in early childhood were more likely to develop asthma during the following 5-year period when compared with children living in homes without such flooring material. A similar association could be seen for children with autism spectrum disorder, where PVC-flooring in early childhood was associated with more reports of autism spectrum disorder five years later. These results indicate that building materials including suspected endocrine disrupting chemicals such as phthalates might be of importance for the development of these chronic diseases. Further studies are needed to explore the early life exposure and the mechanisms and contribution of phthalates for the development of chronic diseases. / Appendix A (en undersökning) och Appendix B (en undersökning)finns i den tryckta versionen av avhandlingen

In this thesis, I examine the politics, poetics, and logics of uneventful human harm in the United States by tracking the life and afterlife of a chemically contaminated emergency housing unit. In 2005, the Federal Emergency Management Agency (FEMA) deployed 120,000 trailers to the US Gulf Coast to house those displaced by Hurricanes Katrina and Rita. Chemical testing, spurred by reports of inhabitant illness, revealed elevated levels of formaldehyde emanating from the plywood walls of the trailers. After being reclaimed by the federal government and beginning in 2010, the FEMA trailers were resold at auction to every corner of the country. Resold trailers gravitated to precarious populations at the poles of rural capital accumulation—from oil patches in North Dakota to reservations in Washington. These trailers serve as an exceptional substrate for an investigation into the anatomy of the uneventful as they once approached the apex of eventfulness as a national controversy and now reside in the shadows of the everyday. This thesis apprehends and theorizes these dispersed and ordinary instruments of domestic harm across multiple registers: epistemological, material, spatial, and affective. I examine how failures of matter and meaning shaped and patterned the lives of those who inhabited the FEMA trailers as their lives became framed by chemical off-gassing, architectural insufficiency, material deterioration, and electrical short-circuiting. Crossing scales and venues, I interrogate the modalities of scientific incomprehension that erode the perception, admittance, or substantiation of mass chemical exposure. These technical processes, along with cultural horizons of eventfulness and the chronicity of disaster, foreclosed avenues of toxic harm accountability. These ‘economies of abandonment’ bring into relief the contemporary biopolitical priorities in which the FEMA trailer—an ostensible protection from harm that fosters illness—becomes possible. FEMA trailer residents attend to the minute, gradual, and ongoing symptoms of exposure to discern the reality and magnitude of residential contamination. The body of the exposed becomes both an epistemic instrument and, across time, the means of making low-level, chronic, and cruddy chemical exposures into eventful instances that drive individuals to action.