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2.  New Link in the Food Chain? Marine Plastic Pollution and Seafood Safety 
Environmental Health Perspectives  2015;123(2):A34-A41.
doi:10.1289/ehp.123-A34
PMCID: PMC4314237  PMID: 25643424
3.  Seeds of Toxicity? Erythrocytes and Lead-Associated Kidney Damage 
doi:10.1289/ehp.123-A42
PMCID: PMC4314238  PMID: 25643425
4.  The View from Afar: Satellite-Derived Estimates of Global PM2.5 
doi:10.1289/ehp.123-A43
PMCID: PMC4314239  PMID: 25643426
7.  Maternal Arsenic Exposure, Arsenic Methylation Efficiency, and Birth Outcomes in the Biomarkers of Exposure to ARsenic (BEAR) Pregnancy Cohort in Mexico 
Environmental Health Perspectives  2014;123(2):186-192.
Background: Exposure to inorganic arsenic (iAs) from drinking water is a global public health problem, yet much remains unknown about the extent of exposure in susceptible populations.
Objectives: We aimed to establish the Biomarkers of Exposure to ARsenic (BEAR) prospective pregnancy cohort in Gómez Palacio, Mexico, to better understand the effects of iAs exposure on pregnant women and their children.
Methods: Two hundred pregnant women were recruited for this study. Concentrations of iAs in drinking water (DW-iAs) and maternal urinary concentrations of iAs and its monomethylated and dimethylated metabolites (MMAs and DMAs, respectively) were determined. Birth outcomes were analyzed for their relationship to DW-iAs and to the concentrations and proportions of maternal urinary arsenicals.
Results: DW-iAs for the study subjects ranged from < 0.5 to 236 μg As/L. More than half of the women (53%) had DW-iAs that exceeded the World Health Organization’s recommended guideline of 10 μg As/L. DW-iAs was significantly associated with the sum of the urinary arsenicals (U-tAs). Maternal urinary concentrations of MMAs were negatively associated with newborn birth weight and gestational age. Maternal urinary concentrations of iAs were associated with lower mean gestational age and newborn length.
Conclusions: Biomonitoring results demonstrate that pregnant women in Gómez Palacio are exposed to potentially harmful levels of DW-iAs. The data support a relationship between iAs metabolism in pregnant women and adverse birth outcomes. The results underscore the risks associated with iAs exposure in vulnerable populations.
Citation: Laine JE, Bailey KA, Rubio-Andrade M, Olshan AF, Smeester L, Drobná Z, Herring AH, Stýblo M, García-Vargas GG, Fry RC. 2015. Maternal arsenic exposure, arsenic methylation efficiency, and birth outcomes in the Biomarkers of Exposure to ARsenic (BEAR) pregnancy cohort in Mexico. Environ Health Perspect 123:186–192; http://dx.doi.org/10.1289/ehp.1307476
doi:10.1289/ehp.1307476
PMCID: PMC4314242  PMID: 25325819
8.  Association between Lifetime Exposure to Inorganic Arsenic in Drinking Water and Coronary Heart Disease in Colorado Residents 
Environmental Health Perspectives  2014;123(2):128-134.
Background: Chronic diseases, including coronary heart disease (CHD), have been associated with ingestion of drinking water with high levels of inorganic arsenic (> 1,000 μg/L). However, associations have been inconclusive in populations with lower levels (< 100 μg/L) of inorganic arsenic exposure.
Objectives: We conducted a case-cohort study based on individual estimates of lifetime arsenic exposure to examine the relationship between chronic low-level arsenic exposure and risk of CHD.
Methods: This study included 555 participants with 96 CHD events diagnosed between 1984 and 1998 for which individual lifetime arsenic exposure estimates were determined using data from structured interviews and secondary data sources to determine lifetime residence, which was linked to a geospatial model of arsenic concentrations in drinking water. These lifetime arsenic exposure estimates were correlated with historically collected urinary arsenic concentrations. A Cox proportional-hazards model with time-dependent CHD risk factors was used to assess the association between time-weighted average (TWA) lifetime exposure to low-level inorganic arsenic in drinking water and incident CHD.
Results: We estimated a positive association between low-level inorganic arsenic exposure and CHD risk [hazard ratio (HR): = 1.38, 95% CI: 1.09, 1.78] per 15 μg/L while adjusting for age, sex, first-degree family history of CHD, and serum low-density lipoprotein levels. The risk of CHD increased monotonically with increasing TWAs for inorganic arsenic exposure in water relative to < 20 μg/L (HR = 1.2, 95% CI: 0.6, 2.2 for 20–30 μg/L; HR = 2.2; 95% CI: 1.2, 4.0 for 30–45 μg/L; and HR = 3, 95% CI: 1.1, 9.1 for 45–88 μg/L).
Conclusions: Lifetime exposure to low-level inorganic arsenic in drinking water was associated with increased risk for CHD in this population.
Citation: James KA, Byers T, Hokanson JE, Meliker JR, Zerbe GO, Marshall JA. 2015. Association between lifetime exposure to inorganic arsenic in drinking water and coronary heart disease in Colorado residents. Environ Health Perspect 123:128–134; http://dx.doi.org/10.1289/ehp.1307839
doi:10.1289/ehp.1307839
PMCID: PMC4314243  PMID: 25350952
9.  Air Pollution and Percent Emphysema Identified by Computed Tomography in the Multi-Ethnic Study of Atherosclerosis 
Environmental Health Perspectives  2014;123(2):144-151.
Background: Air pollution is linked to low lung function and to respiratory events, yet little is known of associations with lung structure.
Objectives: We examined associations of particulate matter (PM2.5, PM10) and nitrogen oxides (NOx) with percent emphysema-like lung on computed tomography (CT).
Methods: The Multi-Ethnic Study of Atherosclerosis (MESA) recruited participants (45–84 years of age) in six U.S. states. Percent emphysema was defined as lung regions < –910 Hounsfield Units on cardiac CT scans acquired following a highly standardized protocol. Spirometry was also conducted on a subset. Individual-level 1- and 20-year average air pollution exposures were estimated using spatiotemporal models that included cohort-specific measurements. Multivariable regression was conducted to adjust for traditional risk factors and study location.
Results: Among 6,515 participants, we found evidence of an association between percent emphysema and long-term pollution concentrations in an analysis leveraging between-city exposure contrasts. Higher concentrations of PM2.5 (5 μg/m3) and NOx (25 ppb) over the previous year were associated with 0.6 (95% CI: 0.1, 1.2%) and 0.5 (95% CI: 0.1, 0.9%) higher average percent emphysema, respectively. However, after adjustment for study site the associations were –0.6% (95% CI: –1.5, 0.3%) for PM2.5 and –0.5% (95% CI: –1.1, 0.02%) for NOx. Lower lung function measures (FEV1 and FVC) were associated with higher PM2.5 and NOx levels in 3,791 participants before and after adjustment for study site, though most associations were not statistically significant.
Conclusions: Associations between ambient air pollution and percentage of emphysema-like lung were inconclusive in this cross-sectional study, thus longitudinal analyses may better clarify these associations with percent emphysema.
Citation: Adar SD, Kaufman JD, Diez-Roux AV, Hoffman EA, D’Souza J, Stukovsky KH, Rich SS, Rotter JI, Guo X, Raffel LJ, Sampson PD, Oron AP, Raghunathan T, Barr RG. 2015. Air pollution and percent emphysema identified by computed tomography in the Multi-Ethnic Study of Atherosclerosis. Environ Health Perspect 123:144–151; http://dx.doi.org/10.1289/ehp.1307951
doi:10.1289/ehp.1307951
PMCID: PMC4314244  PMID: 25302408
10.  Human Health Effects of Dichloromethane: Key Findings and Scientific Issues 
Environmental Health Perspectives  2014;123(2):114-119.
Background: The U.S. EPA’s Integrated Risk Information System (IRIS) completed an updated toxicological review of dichloromethane in November 2011.
Objectives: In this commentary we summarize key results and issues of this review, including exposure sources, identification of potential health effects, and updated physiologically based pharmacokinetic (PBPK) modeling.
Methods: We performed a comprehensive review of primary research studies and evaluation of PBPK models.
Discussion: Hepatotoxicity was observed in oral and inhalation exposure studies in several studies in animals; neurological effects were also identified as a potential area of concern. Dichloromethane was classified as likely to be carcinogenic in humans based primarily on evidence of carcinogenicity at two sites (liver and lung) in male and female B6C3F1 mice (inhalation exposure) and at one site (liver) in male B6C3F1 mice (drinking-water exposure). Recent epidemiologic studies of dichloromethane (seven studies of hematopoietic cancers published since 2000) provide additional data raising concerns about associations with non-Hodgkin lymphoma and multiple myeloma. Although there are gaps in the database for dichloromethane genotoxicity (i.e., DNA adduct formation and gene mutations in target tissues in vivo), the positive DNA damage assays correlated with tissue and/or species availability of functional glutathione S-transferase (GST) metabolic activity, the key activation pathway for dichloromethane-induced cancer. Innovations in the IRIS assessment include estimation of cancer risk specifically for a presumed sensitive genotype (GST-theta-1+/+), and PBPK modeling accounting for human physiological distributions based on the expected distribution for all individuals 6 months to 80 years of age.
Conclusion: The 2011 IRIS assessment of dichloromethane provides insights into the toxicity of a commonly used solvent.
Citation: Schlosser PM, Bale AS, Gibbons CF, Wilkins A, Cooper GS. 2015. Human health effects of dichloromethane: key findings and scientific issues. Environ Health Perspect 123:114–119; http://dx.doi.org/10.1289/ehp.1308030
doi:10.1289/ehp.1308030
PMCID: PMC4314245  PMID: 25325283
11.  Erythrophagocytosis of Lead-Exposed Erythrocytes by Renal Tubular Cells: Possible Role in Lead-Induced Nephrotoxicity 
Environmental Health Perspectives  2014;123(2):120-127.
Background: Nephrotoxicity associated with lead poisoning has been frequently reported in epidemiological studies, but the underlying mechanisms have not been fully described.
Objectives: We examined the role of erythrocytes, one of the major lead reservoirs, in lead-associated nephrotoxicity.
Methods and results: Co-incubation of lead-exposed human erythrocytes with HK-2 human renal proximal tubular cells resulted in renal tubular cytotoxicity, suggesting a role of erythrocytes in lead-induced nephrotoxicity. Morphological and flow cytometric analyses revealed that HK-2 cells actively phagocytized lead-exposed erythrocytes, which was associated with phosphatidylserine (PS) externalization on the erythrocyte membrane and generation of PS-bearing microvesicles. Increased oxidative stress and up-regulation of nephrotoxic biomarkers, such as NGAL, were observed in HK-2 cells undergoing erythrophagocytosis. Moreover, TGF-β, a marker of fibrosis, was also significantly up-regulated. We examined the significance of erythrophagocytosis in lead-induced nephrotoxicity in rats exposed to lead via drinking water for 12 weeks. We observed iron deposition and generation of oxidative stress in renal tissues of lead-exposed rats, as well as the histopathological alterations such as tubulointerstitial lesions, fibrosis, and up-regulation of KIM-1, NGAL, and TGF-β.
Conclusions: Our data strongly suggest that erythrophagocytosis and subsequent iron deposition in renal tubular cells could significantly enhance nephrotoxicity following lead exposure, providing insight on lead-associated kidney damages.
Citation: Kwon SY, Bae ON, Noh JY, Kim K, Kang S, Shin YJ, Lim KM, Chung JH. 2015. Erythrophagocytosis of lead-exposed erythrocytes by renal tubular cells: possible role in lead-induced nephrotoxicity. Environ Health Perspect 123:120–127; http://dx.doi.org/10.1289/ehp.1408094
doi:10.1289/ehp.1408094
PMCID: PMC4314246  PMID: 25302504
12.  A Prospective Study of Growth and Biomarkers of Exposure to Aflatoxin and Fumonisin during Early Childhood in Tanzania 
Environmental Health Perspectives  2014;123(2):173-178.
Background: Aflatoxin and fumonisin are toxic food contaminants. Knowledge about effects of their exposure and coexposure on child growth is inadequate.
Objective: We investigated the association between child growth and aflatoxin and fumonisin exposure in Tanzania.
Methods: A total of 166 children were recruited at 6–14 months of age and studied at recruitment, and at the 6th and 12th month following recruitment. Blood and urine samples were collected and analyzed for plasma aflatoxin–albumin adducts (AF-alb) using ELISA, and urinary fumonisin B1 (UFB1) using liquid chromatography–mass spectrometry, respectively. Anthropometric measurements were taken, and growth index z-scores were computed.
Results: AF-alb geometric mean concentrations (95% CIs) were 4.7 (3.9, 5.6), 12.9 (9.9, 16.7), and 23.5 (19.9, 27.7) pg/mg albumin at recruitment, 6 months, and 12 months from recruitment, respectively. At these respective sampling times, geometric mean UFB1 concentrations (95% CI) were 313.9 (257.4, 382.9), 167.3 (135.4, 206.7), and 569.5 (464.5, 698.2) pg/mL urine, and the prevalence of stunted children was 44%, 55%, and 56%, respectively. UFB1 concentrations at recruitment were negatively associated with length-for-age z-scores (LAZ) at 6 months (p = 0.016) and at 12 months from recruitment (p = 0.014). The mean UFB1 of the three sampling times (at recruitment and at 6 and 12 months from recruitment) in each child was negatively associated with LAZ (p < 0.001) and length velocity (p = 0.004) at 12 months from recruitment. The negative association between AF-alb and child growth did not reach statistical significance.
Conclusions: Exposure to fumonisin alone or coexposure with aflatoxins may contribute to child growth impairment.
Citation: Shirima CP, Kimanya ME, Routledge MN, Srey C, Kinabo JL, Humpf HU, Wild CP, Tu YK, Gong YY. 2015. A prospective study of growth and biomarkers of exposure to aflatoxin and fumonisin during early childhood in Tanzania. Environ Health Perspect 123:173–178; http://dx.doi.org/10.1289/ehp.1408097
doi:10.1289/ehp.1408097
PMCID: PMC4314247  PMID: 25325363
13.  Early-life Exposure to Organophosphate Pesticides and Pediatric Respiratory Symptoms in the CHAMACOS Cohort 
Environmental Health Perspectives  2014;123(2):179-185.
Background: Although pesticide use is widespread, the possible effect of early-life exposure to organophosphate (OP) on pediatric respiratory health is not well described.
Objectives: We investigated the relationship between early-life exposure to OPs and respiratory outcomes.
Methods: Participants included 359 mothers and children from the CHAMACOS birth cohort. Dialkyl phosphate (DAP) metabolites of OP pesticides, specifically diethyl (DE) and dimethyl (DM) phosphate metabolites, were measured in urine from mothers twice during pregnancy (mean = 13 and 26 weeks gestation) and from children five times during childhood (0.5–5 years). Childhood DAP concentrations were estimated by the area under curve (AUC). Mothers reported their child’s respiratory symptoms at 5 and 7 years of age. We used generalized estimating equations (GEE) to examine associations of prenatal and childhood DAP concentrations with repeated measures of respiratory symptoms and exercise-induced coughing at 5 and 7 years of age, adjusting for child’s sex and age, maternal smoking during pregnancy, secondhand tobacco smoke, season of birth, PM2.5, breastfeeding, mold and cockroaches in home, and distance from highway.
Results: Higher prenatal DAP concentrations, particularly DE, were nonsignificantly associated with respiratory symptoms in the previous 12 months at 5 or 7 years of age [adjusted odds ratio (aOR) per 10-fold increase = 1.44; 95% CI: 0.98, 2.12]. This association was strongest with total DAP and DE from the second half of pregnancy (aOR per 10-fold increase = 1.77; 95% CI: 1.06, 2.95; and 1.61; 95% CI: 1.08, 2.39, respectively). Childhood DAP, DE, and DM concentrations were associated with respiratory symptoms and exercise-induced coughing in the previous 12 months at 5 or 7 years of age (total DAPs: aOR per 10-fold increase = 2.53; 95% CI: 1.32, 4.86; and aOR = 5.40; 95% CI: 2.10, 13.91, respectively).
Conclusions: Early-life exposure to OP pesticides was associated with respiratory symptoms consistent with possible asthma in childhood.
Citation: Raanan R, Harley KG, Balmes JR, Bradman A, Lipsett M, Eskenazi B. 2015. Early-life exposure to organophosphate pesticides and pediatric respiratory symptoms in the CHAMACOS cohort. Environ Health Perspect 123:179–185; http://dx.doi.org/10.1289/ehp.1408235
doi:10.1289/ehp.1408235
PMCID: PMC4314248  PMID: 25369257
14.  Characterizing the Peroxisome Proliferator-Activated Receptor (PPARγ) Ligand Binding Potential of Several Major Flame Retardants, Their Metabolites, and Chemical Mixtures in House Dust 
Environmental Health Perspectives  2014;123(2):166-172.
Background: Accumulating evidence has shown that some environmental contaminants can alter adipogenesis and act as obesogens. Many of these contaminants act via the activation of the peroxisome proliferator-activated receptor γ (PPARγ) nuclear receptor.
Objectives: Our goal was to determine the PPARγ ligand binding potency of several major flame retardants, including polybrominated diphenyl ethers (PBDEs), halogenated phenols and bisphenols, and their metabolites. Ligand binding activity of indoor dust and its bioactivated extracts were also investigated.
Methods: We used a commercially available fluorescence polarization ligand binding assay to investigate the binding potency of flame retardants and dust extracts to human PPARγ ligand-binding domain. Rosiglitazone was used as a positive control.
Results: Most of the tested compounds exhibited dose-dependent binding to PPARγ. Mono(2-ethylhexyl) tetrabromophthalate, halogenated bisphenols and phenols, and hydroxylated PBDEs were found to be potent PPARγ ligands. The most potent compound was 3-OH-BDE-47, with an IC50 (concentration required to reduce effect by 50%) of 0.24 μM. The extent of halogenation and the position of the hydroxyl group strongly affected binding. In the dust samples, 21 of the 24 samples tested showed significant binding potency at a concentration of 3 mg dust equivalent (DEQ)/mL. A 3–16% increase in PPARγ binding potency was observed following bioactivation of the dust using rat hepatic S9 fractions.
Conclusion: Our results suggest that several flame retardants are potential PPARγ ligands and that metabolism may lead to increased binding affinity. The PPARγ binding activity of house dust extracts at levels comparable to human exposure warrants further studies into agonistic or antagonistic activities and their potential health effects.
Citation: Fang M, Webster TF, Ferguson PL, Stapleton HM. 2015. Characterizing the peroxisome proliferator-activated receptor (PPARγ) ligand binding potential of several major flame retardants, their metabolites, and chemical mixtures in house dust. Environ Health Perspect 123:166–172; http://dx.doi.org/10.1289/ehp.1408522
doi:10.1289/ehp.1408522
PMCID: PMC4314249  PMID: 25314719
15.  Evaluating Health Risks from Inhaled Polychlorinated Biphenyls: Research Needs for Addressing Uncertainty 
Environmental Health Perspectives  2014;123(2):109-113.
Background: Indoor air concentrations of polychlorinated biphenyls (PCBs) in some buildings are one or more orders of magnitude higher than background levels. In response to this, efforts have been made to assess the potential health risk posed by inhaled PCBs. These efforts are hindered by uncertainties related to the characterization and assessment of source, exposure, and exposure-response.
Objectives: We briefly describe some common sources of PCBs in indoor air and estimate the contribution of inhalation exposure to total PCB exposure for select age groups. Next, we identify critical areas of research needed to improve assessment of exposure and exposure response for inhaled PCBs.
Discussion: Although the manufacture of PCBs was banned in the United States in 1979, many buildings constructed before then still contain potential sources of indoor air PCB contamination. In some indoor settings and for some age groups, inhalation may contribute more to total PCB exposure than any other route of exposure. PCB exposure has been associated with human health effects, but data specific to the inhalation route are scarce. To support exposure–response assessment, it is critical that future investigations of the health impacts of PCB inhalation carefully consider certain aspects of study design, including characterization of the PCB mixture present.
Conclusions: In certain contexts, inhalation exposure to PCBs may contribute more to total PCB exposure than previously assumed. New epidemiological and toxicological studies addressing the potential health impacts of inhaled PCBs may be useful for quantifying exposure–response relationships and evaluating risks.
Citation: Lehmann GM, Christensen K, Maddaloni M, Phillips LJ. 2015. Evaluating health risks from inhaled polychlorinated biphenyls: research needs for addressing uncertainty. Environ Health Perspect 123:109–113; http://dx.doi.org/10.1289/ehp.1408564
doi:10.1289/ehp.1408564
PMCID: PMC4314250  PMID: 25302536
16.  Prenatal Exposure to Maternal Cigarette Smoking and DNA Methylation: Epigenome-Wide Association in a Discovery Sample of Adolescents and Replication in an Independent Cohort at Birth through 17 Years of Age 
Environmental Health Perspectives  2014;123(2):193-199.
Background: Prenatal exposure to maternal cigarette smoking (prenatal smoke exposure) had been associated with altered DNA methylation (DNAm) at birth.
Objective: We examined whether such alterations are present from birth through adolescence.
Methods: We used the Infinium HumanMethylation450K BeadChip to search across 473,395 CpGs for differential DNAm associated with prenatal smoke exposure during adolescence in a discovery cohort (n = 132) and at birth, during childhood, and during adolescence in a replication cohort (n = 447).
Results: In the discovery cohort, we found five CpGs in MYO1G (top-ranking CpG: cg12803068, p = 3.3 × 10–11) and CNTNAP2 (cg25949550, p = 4.0 × 10–9) to be differentially methylated between exposed and nonexposed individuals during adolescence. The CpGs in MYO1G and CNTNAP2 were associated, respectively, with higher and lower DNAm in exposed versus nonexposed adolescents. The same CpGs were differentially methylated at birth, during childhood, and during adolescence in the replication cohort. In both cohorts and at all developmental time points, the differential DNAm was in the same direction and of a similar magnitude, and was not altered appreciably by adjustment for current smoking by the participants or their parents. In addition, four of the five EWAS (epigenome-wide association study)–significant CpGs in the adolescent discovery cohort were also among the top sites of differential methylation in a previous birth cohort, and differential methylation of CpGs in CYP1A1, AHRR, and GFI1 observed in that study was also evident in our discovery cohort.
Conclusions: Our findings suggest that modifications of DNAm associated with prenatal maternal smoking may persist in exposed offspring for many years—at least until adolescence.
Citation: Lee KW, Richmond R, Hu P, French L, Shin J, Bourdon C, Reischl E, Waldenberger M, Zeilinger S, Gaunt T, McArdle W, Ring S, Woodward G, Bouchard L, Gaudet D, Davey Smith G, Relton C, Paus T, Pausova Z. 2015. Prenatal exposure to maternal cigarette smoking and DNA methylation: epigenome-wide association in a discovery sample of adolescents and replication in an independent cohort at birth through 17 years of age. Environ Health Perspect 123:193–199; http://dx.doi.org/10.1289/ehp.1408614
doi:10.1289/ehp.1408614
PMCID: PMC4314251  PMID: 25325234
17.  Use of Satellite Observations for Long-Term Exposure Assessment of Global Concentrations of Fine Particulate Matter 
Environmental Health Perspectives  2014;123(2):135-143.
Background: More than a decade of satellite observations offers global information about the trend and magnitude of human exposure to fine particulate matter (PM2.5).
Objective: In this study, we developed improved global exposure estimates of ambient PM2.5 mass and trend using PM2.5 concentrations inferred from multiple satellite instruments.
Methods: We combined three satellite-derived PM2.5 sources to produce global PM2.5 estimates at about 10 km × 10 km from 1998 through 2012. For each source, we related total column retrievals of aerosol optical depth to near-ground PM2.5 using the GEOS–Chem chemical transport model to represent local aerosol optical properties and vertical profiles. We collected 210 global ground-based PM2.5 observations from the literature to evaluate our satellite-based estimates with values measured in areas other than North America and Europe.
Results: We estimated that global population-weighted ambient PM2.5 concentrations increased 0.55 μg/m3/year (95% CI: 0.43, 0.67) (2.1%/year; 95% CI: 1.6, 2.6) from 1998 through 2012. Increasing PM2.5 in some developing regions drove this global change, despite decreasing PM2.5 in some developed regions. The estimated proportion of the population of East Asia living above the World Health Organization (WHO) Interim Target-1 of 35 μg/m3 increased from 51% in 1998–2000 to 70% in 2010–2012. In contrast, the North American proportion above the WHO Air Quality Guideline of 10 μg/m3 fell from 62% in 1998–2000 to 19% in 2010–2012. We found significant agreement between satellite-derived estimates and ground-based measurements outside North America and Europe (r = 0.81; n = 210; slope = 0.68). The low bias in satellite-derived estimates suggests that true global concentrations could be even greater.
Conclusions: Satellite observations provide insight into global long-term changes in ambient PM2.5 concentrations. Satellite-derived estimates and ground-based PM2.5 observations from this study are available for public use.
Citation: van Donkelaar A, Martin RV, Brauer M, Boys BL. 2015. Use of satellite observations for long-term exposure assessment of global concentrations of fine particulate matter. Environ Health Perspect 123:135–143; http://dx.doi.org/10.1289/ehp.1408646
doi:10.1289/ehp.1408646
PMCID: PMC4314252  PMID: 25343779
18.  Monitoring Indoor Exposure to Organophosphate Flame Retardants: Hand Wipes and House Dust 
Environmental Health Perspectives  2014;123(2):160-165.
Background: Organophosphate flame retardants (PFRs) are becoming popular replacements for the phased-out polybrominated diphenyl ether (PBDE) mixtures, and they are now commonly detected in indoor environments. However, little is known about human exposure to PFRs because they cannot be easily measured in blood or serum.
Objectives: To investigate relationships between the home environment and internal exposure, we assessed associations between two PFRs, tris(1,3-dichloropropyl) phosphate (TDCIPP) and triphenyl phosphate (TPHP), in paired hand wipe and dust samples and concentrations of their metabolites in urine samples (n = 53). We also assessed short-term variation in urinary metabolite concentrations (n = 11 participants; n = 49 samples).
Methods: Adult volunteers in North Carolina, USA, completed questionnaires and provided urine, hand wipe, and household dust samples. PFRs and PBDEs were measured in hand wipes and dust, and bis(1,3-dichloropropyl) phosphate (BDCIPP) and diphenyl phosphate (DPHP), metabolites of TDCIPP and TPHP, were measured in urine.
Results: TDCIPP and TPHP were detected frequently in hand wipes and dust (> 86.8%), with geometric mean concentrations exceeding those of PBDEs. Unlike PBDEs, dust TDCIPP and TPHP levels were not associated with hand wipes. However, hand wipe levels were associated with urinary metabolites. Participants with the highest hand wipe TPHP mass, for instance, had DPHP levels 2.42 times those of participants with the lowest levels (95% CI: 1.23, 4.77). Women had higher levels of DPHP, but not BDCIPP. BDCIPP and DPHP concentrations were moderately to strongly reliable over 5 consecutive days (intraclass correlation coefficients of 0.81 and 0.51, respectively).
Conclusions: PFR exposures are widespread, and hand-to-mouth contact or dermal absorption may be important pathways of exposure.
Citation: Hoffman K, Garantziotis S, Birnbaum LS, Stapleton HM. 2015. Monitoring indoor exposure to organophosphate flame retardants: hand wipes and house dust. Environ Health Perspect 123:160–165; http://dx.doi.org/10.1289/ehp.1408669
doi:10.1289/ehp.1408669
PMCID: PMC4314253  PMID: 25343780
19.  A Targeted Health Risk Assessment Following the Deepwater Horizon Oil Spill: Polycyclic Aromatic Hydrocarbon Exposure in Vietnamese-American Shrimp Consumers 
Environmental Health Perspectives  2014;123(2):152-159.
Background: The Deepwater Horizon oil spill of 2010 prompted concern about health risks among seafood consumers exposed to polycyclic aromatic hydrocarbons (PAHs) via consumption of contaminated seafood.
Objective: The objective of this study was to conduct population-specific probabilistic health risk assessments based on consumption of locally harvested white shrimp (Litopenaeus setiferus) among Vietnamese Americans in southeast Louisiana.
Methods: We conducted a survey of Vietnamese Americans in southeast Louisiana to evaluate shrimp consumption, preparation methods, and body weight among shrimp consumers in the disaster-impacted region. We also collected and chemically analyzed locally harvested white shrimp for 81 individual PAHs. We combined the PAH levels (with accepted reference doses) found in the shrimp with the survey data to conduct Monte Carlo simulations for probabilistic noncancer health risk assessments. We also conducted probabilistic cancer risk assessments using relative potency factors (RPFs) to estimate cancer risks from the intake of PAHs from white shrimp.
Results: Monte Carlo simulations were used to generate hazard quotient distributions for noncancer health risks, reported as mean ± SD, for naphthalene (1.8 × 10–4 ± 3.3 × 10–4), fluorene (2.4 × 10–5 ± 3.3 × 10–5), anthracene (3.9 × 10–6 ± 5.4 × 10–6), pyrene (3.2 × 10–5 ± 4.3 × 10–5), and fluoranthene (1.8 × 10–4 ± 3.3 × 10–4). A cancer risk distribution, based on RPF-adjusted PAH intake, was also generated (2.4 × 10–7 ± 3.9 × 10–7).
Conclusions: The risk assessment results show no acute health risks or excess cancer risk associated with consumption of shrimp containing the levels of PAHs detected in our study, even among frequent shrimp consumers.
Citation: Wilson MJ, Frickel S, Nguyen D, Bui T, Echsner S, Simon BR, Howard JL, Miller K, Wickliffe JK. 2015. A targeted health risk assessment following the Deepwater Horizon Oil Spill: polycyclic aromatic hydrocarbon exposure in Vietnamese-American shrimp consumers. Environ Health Perspect 123:152–159; http://dx.doi.org/10.1289/ehp.1408684
doi:10.1289/ehp.1408684
PMCID: PMC4314254  PMID: 25333566
22.  In Search of “Just Right”: The Challenge of Regulating Arsenic in Rice 
Environmental Health Perspectives  2015;123(1):A16-A19.
doi:10.1289/ehp.123-A16
PMCID: PMC4286262  PMID: 25561606

Results 1-25 (5307)