| 351. |
- Vestergren, Robin, et al.
(author)
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Dietary exposure to perfluoroalkyl acids for the Swedish population in 1999, 2005 and 2010
- 2012
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In: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 49, s. 120-127
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Journal article (peer-reviewed)abstract
- Dietary intake has been hypothesized to be the major pathway of human exposure to perfluoroalkyl acids (PFAAs). However, difficulties associated with the analysis of PFAAs at ultra trace levels in food samples have prevented the confirmation of this hypothesis. In this study, the dietary intake of PFAAs for the general Swedish population was estimated by applying a highly sensitive analytical method to a set of archived food market basket samples from 1999, 2005 and 2010. Dietary exposure to perfluorooctane sulfonic acid (PFOS) (860-1440 pg kg(-1) day(-1)), perfluoroundecanoic acid (PFUnDA) (90-210 pg kg(-1) day(-1)), perfluorodecanoic acid (PFDA) (50-110 pg kg(-1) day(-1)) and perfluorononanoic acid (PFNA) (70-80 pg kg(-1) day(-1)) was dominated by the consumption of fish and meat. In contrast, dietary exposure to PFOA (350-690 pg kg(-1) day(-1)) originated from low levels (8-62 pg g(-1)) found in several high consumption food categories including cereals, dairy products, vegetables and fruit. The dietary intakes of PFOS and PFOA estimated in this study were 4 to 10 times lower compared to previous exposure modeling studies. Nevertheless, the dietary intake of PFOS and PFOA was still a factor of 6 to 10 higher than exposure through ingestion of household dust and drinking water estimated for the general Swedish population. For perfluorohexanoic acid (PFHxA), perfluoroheptanoic acid (PFHpA) and perfluorohexane sulfonic acid (PFHxS) drinking water intake was the major exposure pathway (36-53% of the total exposure) whereas dust ingestion made a significant contribution (27-49%) to the total exposure for PFHxA, PFHpA, PFNA, perfluorotridecanoic acid (PFTrDA) and perfluorotetradecanoic acid (PFTeDA). Dietary intakes varied by less than a factor of three for all PFAAs during the different sampling years which demonstrates that dietary intake has been fairly constant over the past decade when many manufacturing changes occurred.
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| 352. |
- Vestergren, Robin
(author)
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Historical human exposure to perfluoroalkyl acids in the United States and Australia reconstructed from biomonitoring data using population-based pharmacokinetic modelling
- 2018
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In: Environment International. - 0160-4120 .- 1873-6750. ; 92-102:108
-
Journal article (peer-reviewed)abstract
- Perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS) and perfluorohexanesulfonic acid (PFHxS) are found in the blood of humans and wildlife worldwide. Since the beginning of the 21st century, a downward trend in the human body burden, especially for PFOS and PFOA, has been observed while there is no clear temporal trend in wildlife. The inconsistency between the concentration decline in human serum and in wildlife could be indicative of a historical exposure pathway for humans linked to consumer products that has been reduced or eliminated. In this study, we reconstruct the past human exposure trends in two different regions, USA and Australia, by inferring the historical intake from cross-sectional biomonitoring data of PFOS, PFOA and PFHxS using a population-based pharmacokinetic model. For PFOS in the USA, the reconstructed daily intake peaked at 4.5ng/kg-bw/day between 1988 and 1999 while in Australia it peaked at 4.0ng/kg-bw/day between 1984 and 1996. For PFOA in the USA and Australia, the peak reconstructed daily intake was 1.1ng/kg-bw/day in 1995 and 3.6ng/kg-bw/day in 1992, respectively, and started to decline in 2000 and 1995, respectively. The model could not be satisfactorily fitted to the biomonitoring data for PFHxS within reasonable boundaries for its intrinsic elimination half-life, and thus reconstructing intakes of PFHxS was not possible. Our results indicate that humans experienced similar exposure levels and trends to PFOS and PFOA in the USA and Australia. Our findings support the hypothesis that near-field consumer product exposure pathways were likely dominant prior to the phase-out in industrialized countries. The intrinsic elimination half-life, which represents elimination processes that are common for all humans, and elimination processes unique to women (i.e., menstruation, cord-blood transfer and breastfeeding) were also investigated. The intrinsic elimination half-lives for PFOS and PFOA derived from model fitting for men were 3.8 and 2.4years, respectively, for the USA, and 4.9 and 2years respectively for Australia. Our results show that menstruation is a depuration pathway for PFOA for women, similarly but to a lesser extent compared to previous reports for PFOS. However menstruation, cord-blood transfer and breastfeeding together do not fully explain the apparently more rapid elimination of PFOA and PFOS by women compared to men; the intrinsic elimination half-lives in women were up to 13% lower for PFOS and up to 12% lower for PFOA compared to the corresponding half-lives in men.
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| 353. |
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| 354. |
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| 355. |
- Vitolo, Claudia, et al.
(author)
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Mapping combined wildfire and heat stress hazards to improve evidence-based decision making
- 2019
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In: Environment International. - : PERGAMON-ELSEVIER SCIENCE LTD. - 0160-4120 .- 1873-6750. ; 127, s. 21-34
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Journal article (peer-reviewed)abstract
- Heat stress and forest fires are often considered highly correlated hazards as extreme temperatures play a key role in both occurrences. This commonality can influence how civil protection and local responders deploy resources on the ground and could lead to an underestimation of potential impacts, as people could be less resilient when exposed to multiple hazards. In this work, we provide a simple methodology to identify areas prone to concurrent hazards, exemplified with, but not limited to, heat stress and fire danger. We use the combined heat and forest fire event that affected Europe in June 2017 to demonstrate that the methodology can be used for analysing past events as well as making predictions, by using reanalysis and medium-range weather forecasts, respectively. We present new spatial layers that map the combined danger and make suggestions on how these could be used in the context of a Multi-Hazard Early Warning System. These products could be particularly valuable in disaster risk reduction and emergency response management, particularly for civil protection, humanitarian agencies and other first responders whose role is to identify priorities during pre-interventions and emergencies.
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| 356. |
- Vuong, Ann M., et al.
(author)
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Polybrominated diphenyl ether (PBDE) exposures and thyroid hormones in children at age 3 years
- 2018
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In: Environment International. - : Elsevier. - 0160-4120 .- 1873-6750. ; 117, s. 339-347
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Journal article (peer-reviewed)abstract
- BACKGROUND: Polybrominated diphenyl ethers (PBDEs) reduce serum thyroid hormone concentrations in animal studies, but few studies have examined the impact of early-life PBDE exposures on thyroid hormone disruption in childhood.METHODS: We used data from 162 mother-child pairs from the Health Outcomes and Measures of the Environment Study (2003-2006, Cincinnati, OH). We measured PBDEs in maternal serum at 16 ± 3 weeks gestation and in child serum at 1-3 years. Thyroid hormones were measured in serum at 3 years. We used multiple informant models to investigate associations between prenatal and early-life PBDE exposures and thyroid hormone levels at age 3 years.RESULTS: Prenatal PBDEs were associated with decreased thyroid stimulating hormone (TSH) levels at age 3 years. A 10-fold increase in prenatal ∑PBDEs (BDE-28, -47, -99, -100, and -153) was associated with a 27.6% decrease (95% CI -40.8%, -11.3%) in TSH. A ten-fold increase in prenatal ∑PBDEs was associated with a 0.25 pg/mL (0.07, 0.43) increase in free triiodothyronine (FT3). Child sex modified associations between prenatal PBDEs and thyroid hormones, with significant decrements in TSH among females and decreased free T4 (FT4) in males. Prenatal ∑PBDEs were not associated with TT4, FT4, or total T3.CONCLUSIONS: These findings suggest an inverse relationship between prenatal ∑PBDEs and TSH at 3 years. Associations may be sexually dimorphic, with an inverse relationship between prenatal BDE-47 and -99 and TSH in females and null associations among males.
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| 357. |
- Wahlberg, Karin, et al.
(author)
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Maternal polymorphisms in glutathione-related genes are associated with maternal mercury concentrations and early child neurodevelopment in a population with a fish-rich diet
- 2018
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In: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 115, s. 142-149
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Journal article (peer-reviewed)abstract
- Introduction: Glutathione (GSH) pathways play a key role the metabolism and elimination of the neurotoxicant methylmercury (MeHg). We hypothesized that maternal genetic variation linked to GSH pathways could influence MeHg concentrations in pregnant mothers and children and thereby also affect early life development. Methods: The GCLM (rs41303970, C/T), GCLC (rs761142, T/G) and GSTP1 (rs1695, A/G) polymorphisms were genotyped in 1449 mothers in a prospective study of the Seychellois population with a diet rich in fish. Genotypes were analyzed in association with maternal hair and blood Hg, fetal blood Hg (cord blood Hg), as well as children's mental (MDI) and motor development (PDI; MDI and PDI assessed by Bayley Scales of Infant Development at 20 months). We also examined whether genotypes modified the association between Hg exposure and developmental outcomes. Results: GCLC rs761142 TT homozygotes showed statistically higher mean maternal hair Hg (4.12 ppm) than G carriers (AG 3.73 and GG 3.52 ppm) (p = 0.037). For the combination of GCLC rs761142 and GCLM rs41303970, double homozygotes TT + CC showed higher hair Hg (4.40 ppm) than G + T carriers (3.44 ppm; p = 0.018). No associations were observed between GSTP1 rs1695 and maternal hair Hg or between any genotypes and maternal blood Hg or cord blood Hg. The maternal GSTP1 rs1695 rare allele (G) was associated with a lower MDI among children (β = −1.48, p = 0.048). We also observed some interactions: increasing Hg in maternal and cord blood was associated with lower PDI among GCLC rs761142 TT carriers; and increasing Hg in hair was associated with lower MDI among GSTP1 rs1695 GG carriers. Conclusions: Maternal genetic variation in genes involved in GSH synthesis is statistically associated with Hg concentrations in maternal hair, but not in maternal or fetal blood. We observed interactions that suggest maternal GSH genetics may modify associations between MeHg exposure and neurodevelopmental outcomes.
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| 358. |
- Wang, Juan, et al.
(author)
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Asthma, allergic rhinitis and eczema among parents of preschool children in relation to climate, and dampness and mold in dwellings in China
- 2019
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In: Environment International. - : PERGAMON-ELSEVIER SCIENCE LTD. - 0160-4120 .- 1873-6750. ; 130
-
Journal article (peer-reviewed)abstract
- The main aim was to study associations between asthma, allergic rhinitis and eczema among adults across China and dampness and mold at home. Young adults (N = 40,279) in eight cities in China answered a questionnaire in 2010-2012 (response rate 75.0%). Data on asthma, allergic rhinitis, eczema and the home environment was assessed by the questionnaire. Climate data was obtained from China Meteorological Administration and the website of Weather Underground. Health associations were analyzed by two-level logistic regression models, adjusting for covariates. Totally 1.6% had asthma, 6.6% allergic rhinitis and 2.2% eczema. Mold odor was associated with asthma (OR = 1.90) and allergic rhinitis (OR = 1.25-1.44). Window pane condensation in winter was associated with asthma (OR = 1.39), allergic rhinitis (OR = 1.26-1.58) and eczema (OR = 1.36-1.77). Presence of mold spots or damp stains was related to asthma (OR = 1.58-2.49), allergic rhinitis (OR = 1.35-1.76) and eczema (OR = 1.47-1.70). Water damage was related to asthma (OR = 1.69-1.82), allergic rhinitis (OR = 1.40-1.45) and eczema (OR = 1.44-1.96). Damp bed clothing was related to asthma (OR = 1.23), allergic rhinitis (OR = 1.23) and eczema (OR = 1.35). A higher dampness score was associated with increased odds ratios for diseases. Those living in older buildings had more asthma (OR = 1.39-1.76) and allergic rhinitis (OR = 1.16-1.21). Those living in suburban or rural areas had less asthma, allergic rhinitis and eczema as compared to those living in urban areas (OR values from 0.24 to 0.66). Stronger health associations with dampness and mold were found in southern China and in newer buildings (constructed after 2005). In conclusion, dampness and mold at home can be risk factors for asthma, allergic rhinitis and eczema among adults in China. Living in older buildings can be risk factors for asthma or allergic rhinitis while living in less urbanized areas can be protective.
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| 359. |
- Wang, Juan, et al.
(author)
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Dampness and mold at home and at work and onset of insomnia symptoms, snoring and excessive daytime sleepiness
- 2020
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In: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 139
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Journal article (peer-reviewed)abstract
- Aim: To investigate whether exposure to dampness and mold at home and at work induce sleep disturbances and daytime sleepiness among adults. Materials and methods: Associations between onset of sleep disturbances and dampness, mold and mold odor at home and at work were investigated in a cohort of 11,318 adults from the population in Iceland, Norway, Sweden, Denmark and Estonia. The participants answered a questionnaire at baseline and 10 years later, with questions on sleep disturbances, including difficulty initiating sleep (DIS), difficulty maintaining sleep (DMS), early morning awakening (EMA), insomnia symptoms, snoring and excessive daytime sleepiness (EDS). Multiple logistic regression models were applied to estimate associations adjusting for potential confounders including gender, age, smoking habit at baseline, change of smoking habit from baseline to follow up, BMI at baseline, change of BMI from baseline to follow up, education level at follow up, allergic rhinitis at baseline, doctor diagnosed asthma at baseline and chronic bronchitis at baseline. Results: Baseline floor dampness, visible mold and mold odor at home increased onset of DIS, DMS, EMA, insomnia symptoms and snoring during follow up (OR 1.29–1.87). Any sign of dampness at baseline increased onset of DIS (OR 1.28, 95%CI 1.06–1.55), DMS (OR 1.17, 95%CI 1.02–1.34) and insomnia symptoms (OR 1.18, 95%CI 1.03–1.36). Dampness at home during follow up increased onset of DIS, DMS, EMA, insomnia symptoms and EDS (OR 1.17–1.36). Dampness at work during follow up increased onset of DIS, EMA, insomnia symptoms and EDS (OR 1.16–1.34). Combined dampness at home and at work during follow up increased the risk of onset of DIS, DMS, EMA, insomnia symptoms and EDS (OR 1.29–1.74). Conclusions: Dampness and mold at home and at work can increase the development of insomnia symptoms, snoring and EDS among adults. © 2020 The Authors
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| 360. |
- Wang, Meng, et al.
(author)
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Long-term exposure to elemental constituents of particulate matter and cardiovascular mortality in 19 European cohorts : Results from the ESCAPE and TRANSPHORM projects
- 2014
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In: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 66, s. 97-106
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Journal article (peer-reviewed)abstract
- Background: Associations between long-term exposure to ambient particulate matter (PM) and cardiovascular (CVD) mortality have been widely recognized. However, health effects of long-term exposure to constituents of PM on total CVD mortality have been explored in a single study only. Aims: The aim of this study was to examine the association of PM composition with cardiovascular mortality. Methods: We used data from 19 European ongoing cohorts within the framework of the ESCAPE (European Study of Cohorts for Air Pollution Effects) and TRANSPHORM (Transport related Air Pollution and Health impacts Integrated Methodologies for Assessing Particulate Matter) projects. Residential annual average exposure to elemental constituents within particle matter smaller than 2.5 and 10 pm (PM2.5 and PM10) was estimated using Land Use Regression models. Eight elements representing major sources were selected a priori (copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc). Cohort-specific analyses were conducted using Cox proportional hazards models with a standardized protocol. Random-effects metaanalysis was used to calculate combined effect estimates. Results: The total population consisted of 322,291 participants, with 9545 CVD deaths. We found no statistically significant associations between any of the elemental constituents in PM2.5 or PM10 and CVD mortality in the pooled analysis. Most of the hazard ratios (HRs) were close to unity, e.g. for PM10 Fe the combined HR was 0.96 (0.84-1.09). Elevated combined HRs were found for PM2.5 Si (1.17, 95% Cl: 0.93-1.47), and S in PM2.5 (1.08,95% Cl: 0.95-1.22) and PM10 (1.09,95% Cl: 0.90-132). Conclusion: In a joint analysis of 19 European cohorts, we found no statistically significant association between long-term exposure to 8 elemental constituents of particles and total cardiovascular mortality.
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