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Background: There is an increasing awareness of the multiple potential pathways leading to human health risks from hydraulic fracturing. Setback distances are a legislative method to mitigate potential risks.
Objectives: We attempted to determine whether legal setback distances between well-pad sites and the public are adequate in three shale plays.
Methods: We reviewed geography, current statutes and regulations, evacuations, thermal modeling, air pollution studies, and vapor cloud modeling within the Marcellus, Barnett, and Niobrara Shale Plays.
Discussion: The evidence suggests that presently utilized setbacks may leave the public vulnerable to explosions, radiant heat, toxic gas clouds, and air pollution from hydraulic fracturing activities.
Conclusions: Our results suggest that setbacks may not be sufficient to reduce potential threats to human health in areas where hydraulic fracturing occurs. It is more likely that a combination of reasonable setbacks with controls for other sources of pollution associated with the process will be required.
Citation: Haley M, McCawley M, Epstein AC, Arrington B, Bjerke EF. 2016. Adequacy of current state setbacks for directional high-volume hydraulic fracturing in the Marcellus, Barnett, and Niobrara Shale Plays. Environ Health Perspect 124:1323–1333; http://dx.doi.org/10.1289/ehp.1510547
Background: Wildfire activity is predicted to increase in many parts of the world due to changes in temperature and precipitation patterns from global climate change. Wildfire smoke contains numerous hazardous air pollutants and many studies have documented population health effects from this exposure.
Objectives: We aimed to assess the evidence of health effects from exposure to wildfire smoke and to identify susceptible populations.
Methods: We reviewed the scientific literature for studies of wildfire smoke exposure on mortality and on respiratory, cardiovascular, mental, and perinatal health. Within those reviewed papers deemed to have minimal risk of bias, we assessed the coherence and consistency of findings.
Discussion: Consistent evidence documents associations between wildfire smoke exposure and general respiratory health effects, specifically exacerbations of asthma and chronic obstructive pulmonary disease. Growing evidence suggests associations with increased risk of respiratory infections and all-cause mortality. Evidence for cardiovascular effects is mixed, but a few recent studies have reported associations for specific cardiovascular end points. Insufficient research exists to identify specific population subgroups that are more susceptible to wildfire smoke exposure.
Conclusions: Consistent evidence from a large number of studies indicates that wildfire smoke exposure is associated with respiratory morbidity with growing evidence supporting an association with all-cause mortality. More research is needed to clarify which causes of mortality may be associated with wildfire smoke, whether cardiovascular outcomes are associated with wildfire smoke, and if certain populations are more susceptible.
Citation: Reid CE, Brauer M, Johnston FH, Jerrett M, Balmes JR, Elliott CT. 2016. Critical review of health impacts of wildfire smoke exposure. Environ Health Perspect 124:1334–1343; http://dx.doi.org/10.1289/ehp.1409277
Background: Green, natural environments may ameliorate adverse environmental exposures (e.g., air pollution, noise, and extreme heat), increase physical activity and social engagement, and lower stress.
Objectives: We aimed to examine the prospective association between residential greenness and mortality.
Methods: Using data from the U.S.-based Nurses’ Health Study prospective cohort, we defined cumulative average time-varying seasonal greenness surrounding each participant’s address using satellite imagery [Normalized Difference Vegetation Index (NDVI)]. We followed 108,630 women and observed 8,604 deaths between 2000 and 2008.
Results: In models adjusted for mortality risk factors (age, race/ethnicity, smoking, and individual- and area-level socioeconomic status), women living in the highest quintile of cumulative average greenness (accounting for changes in residence during follow-up) in the 250-m area around their home had a 12% lower rate of all-cause nonaccidental mortality [95% confidence interval (CI); 0.82, 0.94] than those in the lowest quintile. The results were consistent for the 1,250-m area, although the relationship was slightly attenuated. These associations were strongest for respiratory and cancer mortality. The findings from a mediation analysis suggested that the association between greenness and mortality may be at least partly mediated by physical activity, particulate matter < 2.5 μm, social engagement, and depression.
Conclusions: Higher levels of green vegetation were associated with decreased mortality. Policies to increase vegetation may provide opportunities for physical activity, reduce harmful exposures, increase social engagement, and improve mental health. Planting vegetation may mitigate the effects of climate change; in addition, evidence of an association between vegetation and lower mortality rates suggests it also might be used to improve health.
Citation: James P, Hart JE, Banay RF, Laden F. 2016. Exposure to greenness and mortality in a nationwide prospective cohort study of women. Environ Health Perspect 124:1344–1352; http://dx.doi.org/10.1289/ehp.1510363
Background: It is unknown if ambient fine particulate matter (PM2.5) is associated with lower renal function, a cardiovascular risk factor.
Objective: We investigated whether long-term PM2.5 exposure was associated with estimated glomerular filtration rate (eGFR) in a cohort of older men living in the Boston Metropolitan area.
Methods: This longitudinal analysis included 669 participants from the Veterans Administration Normative Aging Study with up to four visits between 2000 and 2011 (n = 1,715 visits). Serum creatinine was measured at each visit, and eGFR was calculated according to the Chronic Kidney Disease Epidemiology Collaboration equation. One-year exposure to PM2.5 prior to each visit was assessed using a validated spatiotemporal model that utilized satellite remote-sensing aerosol optical depth data. eGFR was modeled in a time-varying linear mixed-effects regression model as a continuous function of 1-year PM2.5, adjusting for important covariates.
Results: One-year PM2.5 exposure was associated with lower eGFRs; a 2.1-μg/m3 interquartile range higher 1-year PM2.5 was associated with a 1.87 mL/min/1.73 m2 lower eGFR [95% confidence interval (CI): –2.99, –0.76]. A 2.1 μg/m3-higher 1-year PM2.5 was also associated with an additional annual decrease in eGFR of 0.60 mL/min/1.73 m2 per year (95% CI: –0.79, –0.40).
Conclusions: In this longitudinal sample of older men, the findings supported the hypothesis that long-term PM2.5 exposure negatively affects renal function and increases renal function decline.
Citation: Mehta AJ, Zanobetti A, Bind MC, Kloog I, Koutrakis P, Sparrow D, Vokonas PS, Schwartz JD. 2016. Long-term exposure to ambient fine particulate matter and renal function in older men: the VA Normative Aging Study. Environ Health Perspect 124:1353–1360; http://dx.doi.org/10.1289/ehp.1510269
Background: Mild cognitive impairment (MCI) describes the intermediate state between normal cognitive aging and dementia. Adverse effects of air pollution (AP) on cognitive functions have been proposed, but investigations of simultaneous exposure to noise are scarce.
Objectives: We analyzed the cross-sectional associations of long-term exposure to AP and traffic noise with overall MCI and amnestic (aMCI) and nonamnestic (naMCI) MCI.
Methods: At the second examination of the population-based Heinz Nixdorf Recall study, cognitive assessment was completed in 4,086 participants who were 50–80 years old. Of these, 592 participants were diagnosed as having MCI (aMCI, n = 309; naMCI, n = 283) according to previously published criteria using five neuropsychological subtests. We assessed long-term residential concentrations for size-fractioned particulate matter (PM) and nitrogen oxides with land use regression, and for traffic noise [weighted 24-hr (LDEN) and night-time (LNIGHT) means]. Logistic regression models adjusted for individual risk factors were calculated to estimate the association of environmental exposures with MCI in single- and two-exposure models.
Results: Most air pollutants and traffic noise were associated with overall MCI and aMCI. For example, an interquartile range increase in PM2.5 and a 10 A-weighted decibel [dB(A)] increase in LDEN were associated with overall MCI as follows [odds ratio (95% confidence interval)]: 1.16 (1.05, 1.27) and 1.40 (1.03, 1.91), respectively, and with aMCI as follows: 1.22 (1.08, 1.38) and 1.53 (1.05, 2.24), respectively. In two-exposure models, AP and noise associations were attenuated [e.g., for aMCI, PM2.5 1.13 (0.98, 1.30) and LDEN 1.46 (1.11, 1.92)].
Conclusions: Long-term exposures to air pollution and traffic noise were positively associated with MCI, mainly with the amnestic subtype.
Citation: Tzivian L, Dlugaj M, Winkler A, Weinmayr G, Hennig F, Fuks KB, Vossoughi M, Schikowski T, Weimar C, Erbel R, Jöckel KH, Moebus S, Hoffmann B, on behalf of the Heinz Nixdorf Recall study Investigative Group. 2016. Long-term air pollution and traffic noise exposures and mild cognitive impairment in older adults: a cross-sectional analysis of the Heinz Nixdorf Recall Study. Environ Health Perspect 124:1361–1368; http://dx.doi.org/10.1289/ehp.1509824
Background: With its tropical rainforest climate, rapid urbanization, and changing demography and ecology, Singapore experiences endemic dengue; the last large outbreak in 2013 culminated in 22,170 cases. In the absence of a vaccine on the market, vector control is the key approach for prevention.
Objectives: We sought to forecast the evolution of dengue epidemics in Singapore to provide early warning of outbreaks and to facilitate the public health response to moderate an impending outbreak.
Methods: We developed a set of statistical models using least absolute shrinkage and selection operator (LASSO) methods to forecast the weekly incidence of dengue notifications over a 3-month time horizon. This forecasting tool used a variety of data streams and was updated weekly, including recent case data, meteorological data, vector surveillance data, and population-based national statistics. The forecasting methodology was compared with alternative approaches that have been proposed to model dengue case data (seasonal autoregressive integrated moving average and step-down linear regression) by fielding them on the 2013 dengue epidemic, the largest on record in Singapore.
Results: Operationally useful forecasts were obtained at a 3-month lag using the LASSO-derived models. Based on the mean average percentage error, the LASSO approach provided more accurate forecasts than the other methods we assessed. We demonstrate its utility in Singapore’s dengue control program by providing a forecast of the 2013 outbreak for advance preparation of outbreak response.
Conclusions: Statistical models built using machine learning methods such as LASSO have the potential to markedly improve forecasting techniques for recurrent infectious disease outbreaks such as dengue.
Citation: Shi Y, Liu X, Kok SY, Rajarethinam J, Liang S, Yap G, Chong CS, Lee KS, Tan SS, Chin CK, Lo A, Kong W, Ng LC, Cook AR. 2016. Three-month real-time dengue forecast models: an early warning system for outbreak alerts and policy decision support in Singapore. Environ Health Perspect 124:1369–1375; http://dx.doi.org/10.1289/ehp.1509981
Background: Exposure to persistent organic pollutants (POPs) is known to increase risk of diabetes.
Objective: To determine which POPs are most associated with prevalence of diabetes in 601 Akwesasne Native Americans.
Methods: Multiple logistic regression analysis was used to assess associations between quartiles of concentrations of 101 polychlorinated biphenyl (PCBs) congeners, congener groups and three chlorinated pesticides [dichlorodiphenyldichloroethylene (DDE), hexachlorobenzene (HCB) and mirex] with diabetes. In Model 1, the relationship between quartiles of exposure and diabetes were adjusted only for sex, age, body mass index (BMI), and total serum lipids. Model 2 included additional adjustment for either total PCBs or total pesticides.
Results: Total serum PCB and pesticide concentrations were each significantly associated with prevalence of diabetes when adjusted only for covariates (Model 1), but neither showed a significant OR for highest to lowest quartiles after additional adjustment for the other (Model 2). When applying Model 2 to PCB congener groups and individual pesticides, there were significant omnibus differences between the four quartiles (all ps < 0.042) for most groups, with the exception of penta- and hexachlorobiphenyls, DDE and mirex. However, when comparing highest to lowest quartiles only non- and mono-ortho PCBs [OR = 4.55 (95% CI: 1.48, 13.95)], tri- and tetrachloro PCBs [OR = 3.66 (95% CI: 1.37, –9.78)] and HCB [OR = 2.64 (95% CI: 1.05, 6.61)] showed significant associations with diabetes. Among the non- and mono-ortho congeners, highest to lowest quartile of dioxin TEQs was not significant [OR = 1.82 (95% CI: 0.61, 5.40)] but the OR for the non-dioxin-like congeners was [OR = 5.01 (95% CI: 1.76, 14.24)].
Conclusion: The associations with diabetes after adjustment for other POPs were strongest with the more volatile, non-dioxin-like, low-chlorinated PCB congeners and HCB. Because low-chlorinated congeners are more volatile, these observations suggest that inhalation of vapor-phase PCBs is an important route of exposure.
Citation: Aminov Z, Haase R, Rej R, Schymura MJ, Santiago-Rivera A, Morse G, DeCaprio A, Carpenter DO, and the Akwesasne Task Force on the Environment. 2016. Diabetes prevalence in relation to serum concentrations of polychlorinated biphenyl (PCB) congener groups and three chlorinated pesticides in a Native American population. Environ Health Perspect 124:1376–1383; http://dx.doi.org/10.1289/ehp.1509902
Background: Nearly 4.3 million deaths worldwide were attributable to exposure to household air pollution in 2012. However, household coal use remains widespread.
Objectives: We investigated the association of cooking coal and all-cause and cause-specific mortality in a prospective cohort of primarily never-smoking women in Shanghai, China.
Methods: A cohort of 74,941 women were followed from 1996 through 2009 with annual linkage to the Shanghai vital statistics database. Cause-specific mortality was identified through 2009. Use of household coal for cooking was assessed through a residential history questionnaire. Cox proportional hazards models estimated the risk of mortality associated with household coal use.
Results: In this cohort, 63% of the women ever used coal (n = 46,287). Compared with never coal use, ever use of coal was associated with mortality from all causes [hazard ratio (HR) = 1.12; 95% confidence interval (CI): 1.05, 1.21], cancer (HR = 1.14; 95% CI: 1.03, 1.27), and ischemic heart disease (overall HR = 1.61; 95% CI: 1.14, 2.27; HR for myocardial infarction specifically = 1.80; 95% CI: 1.16, 2.79). The risk of cardiovascular mortality increased with increasing duration of coal use, compared with the risk in never users. The association between coal use and ischemic heart disease mortality diminished with increasing years since cessation of coal use.
Conclusions: Evidence from this study suggests that past use of coal among women in Shanghai is associated with excess all-cause mortality, and from cardiovascular diseases in particular. The decreasing association with cardiovascular mortality as the time since last use of coal increased emphasizes the importance of reducing use of household coal where use is still widespread.
Citation: Kim C, Seow WJ, Shu XO, Bassig BA, Rothman N, Chen BE, Xiang YB, Hosgood HD III, Ji BT, Hu W, Wen C, Chow WH, Cai Q, Yang G, Gao YT, Zheng W, Lan Q. 2016. Cooking coal use and all-cause and cause-specific mortality in a prospective cohort study of women in Shanghai, China. Environ Health Perspect 124:1384–1389; http://dx.doi.org/10.1289/EHP236
Background: Epidemiological studies have indicated that noise exposure is associated with an increased risk of type 2 diabetes mellitus (T2DM). However, the nature of the connection between noise exposure and T2DM remains to be explored.
Objectives: We explored whether and how noise exposure affects glucose homeostasis in mice as the initial step toward T2DM development.
Methods: Male ICR mice were randomly assigned to one of four groups: the control group and three noise groups (N20D, N10D, and N1D), in which the animals were exposed to white noise at 95 decibel sound pressure level (dB SPL) for 4 hr per day for 20 successive days, 10 successive days, or 1 day, respectively. Glucose tolerance and insulin sensitivity were evaluated 1 day, 1 week, and 1 month after the final noise exposure (1DPN, 1WPN, and 1MPN). Standard immunoblots, immunohistochemical methods, and enzyme-linked immunosorbent assays (ELISA) were performed to assess insulin signaling in skeletal muscle, the morphology of β cells, and plasma corticosterone levels.
Results: Noise exposure for 1 day caused transient glucose intolerance and insulin resistance, whereas noise exposure for 10 and 20 days had no effect on glucose tolerance but did cause prolonged insulin resistance and an increased insulin response to glucose challenge. Akt phosphorylation and GLUT4 translocation in response to exogenous insulin were decreased in the skeletal muscle of noise-exposed animals.
Conclusions: Noise exposure at 95 dB SPL caused insulin resistance in male ICR mice, which was prolonged with longer noise exposure and was likely related to the observed blunted insulin signaling in skeletal muscle.
Citation: Liu L, Wang F, Lu H, Cao S, Du Z, Wang Y, Feng X, Gao Y, Zha M, Guo M, Sun Z, Wang J. 2016. Effects of noise exposure on systemic and tissue-level markers of glucose homeostasis and insulin resistance in male mice. Environ Health Perspect 124:1390–1398; http://dx.doi.org/10.1289/EHP162
Background: The oxidative phosphorylation system (OXPHOS) includes nuclear chromosome (nDNA)– and mitochondrial DNA (mtDNA)–encoded polypeptides. Many rare OXPHOS disorders, such as striatal necrosis syndromes, are caused by genetic mutations. Despite important advances in sequencing procedures, causative mutations remain undetected in some patients. It is possible that etiologic factors, such as environmental toxins, are the cause of these cases. Indeed, the inhibition of a particular enzyme by a poison could imitate the biochemical effects of pathological mutations in that enzyme. Moreover, environmental factors can modify the penetrance or expressivity of pathological mutations.
Objectives: We studied the interaction between mitochondrially encoded ATP synthase 6 (p.MT-ATP6) subunit and an environmental exposure that may contribute phenotypic differences between healthy individuals and patients suffering from striatal necrosis syndromes or other mitochondriopathies.
Methods: We analyzed the effects of the ATP synthase inhibitor tributyltin chloride (TBTC), a widely distributed environmental factor that contaminates human food and water, on transmitochondrial cell lines with or without an ATP synthase mutation that causes striatal necrosis syndrome. Doses were selected based on TBTC concentrations previously reported in human whole blood samples.
Results: TBTC modified the phenotypic effects caused by a pathological mtDNA mutation. Interestingly, wild-type cells treated with this xenobiotic showed similar bioenergetics when compared with the untreated mutated cells.
Conclusions: In addition to the known genetic causes, our findings suggest that environmental exposure to TBTC might contribute to the etiology of striatal necrosis syndromes.
Citation: López-Gallardo E, Llobet L, Emperador S, Montoya J, Ruiz-Pesini E. 2016. Effects of tributyltin chloride on cybrids with or without an ATP synthase pathologic mutation. Environ Health Perspect 124:1399–1405; http://dx.doi.org/10.1289/EHP182
Background: Although the chlorinated flame retardant Dechlorane (Dec) 602 has been detected in food, human blood, and breast milk, there is limited information on potential health effects, including possible immunotoxicity.
Objectives: We determined the immunotoxic potential of Dec 602 in mice by examining the expression of phenotypic markers on thymocyte and splenic lymphocyte subsets, Th1/Th2 transcription factors, and the production of cytokines and antibodies.
Methods: Adult male C57BL/6 mice were orally exposed to environmentally relevant doses of Dec 602 (1 and 10 μg/kg body weight per day) for 7 consecutive days. Thymocyte and splenic CD4 and CD8 subsets and splenocyte apoptosis were examined by flow cytometric analysis. Cytokine expression was measured at both the mRNA and the protein levels. Levels of the transcription factors Th1 (T-bet and STAT1) and Th2 (GATA3) were determined using quantitative real-time polymerase chain reaction (qPCR). Serum levels of immunoglobulins IgG1, IgG2a, IgG2b and IgE were measured by enzyme-linked immunosorbent assay (ELISA).
Results: Splenic CD4+ and CD8+ T cell subsets were decreased compared with vehicle controls, and apoptosis was significantly increased in splenic CD4+ T cells. Expression (mRNA and protein) of Th2 cytokines [interleukin (IL)-4, IL-10, and IL-13] increased, and that of Th1 cytokines [IL-2, interferon (IFN)-γ and tumor necrosis factor (TNF)-α] decreased. The Th2 transcriptional factor GATA3 increased, whereas the Th1 transcriptional factors T-bet and STAT1 decreased. As additional indicators of the Th2-Th1 imbalance, production of IgG1 was significantly increased, whereas IgG2a was reduced.
Conclusions: To our knowledge, we are the first to report evidence of the effects of Dec 602 on immune function in mice, with findings indicating that Dec 602 exposure favored Th2 responses and reduced Th1 function.
Citation: Feng Y, Tian J, Xie HQ, She J, Xu SL, Xu T, Tian W, Fu H, Li S, Tao W, Wang L, Chen Y, Zhang S, Zhang W, Guo TL, Zhao B. 2016. Effects of acute low-dose exposure to the chlorinated flame retardant dechlorane 602 and Th1 and Th2 immune responses in adult male mice. Environ Health Perspect 124:1406–1413; http://dx.doi.org/10.1289/ehp.1510314
Background: Studies have suggested associations between elevated blood pressure and short-term air pollution exposures, but the evidence is mixed regarding long-term exposures on incidence of hypertension.
Objectives: We examined the association of hypertension incidence with long-term residential exposures to ambient particulate matter (PM) and residential distance to roadway.
Methods: We estimated 24-month and cumulative average exposures to PM10, PM2.5, and PM2.5–10 and residential distance to road for women participating in the prospective nationwide Nurses’ Health Study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated for incident hypertension from 1988 to 2008 using Cox proportional hazards models adjusted for potential confounders. We considered effect modification by age, diet, diabetes, obesity, region, and latitude.
Results: Among 74,880 participants, 36,812 incident cases of hypertension were observed during 960,041 person-years. In multivariable models, 10-μg/m3 increases in 24-month average PM10, PM2.5, and PM2.5–10 were associated with small increases in the incidence of hypertension (HR: 1.02, 95% CI: 1.00, 1.04; HR: 1.04, 95% CI: 1.00, 1.07; and HR: 1.03, 95% CI: 1.00, 1.07, respectively). Associations were stronger among women < 65 years of age (HR: 1.04, 95% CI: 1.01, 1.06; HR: 1.07, 95% CI: 1.02, 1.12; and HR: 1.05, 95% CI: 1.01, 1.09, respectively) and the obese (HR: 1.07, 95% CI: 1.04, 1.12; HR: 1.15, 95% CI: 1.07, 1.23; and HR: 1.13, 95% CI: 1.07, 1.19, respectively), with p-values for interaction < 0.05 for all models except age and PM2.5–10. There was no association with roadway proximity.
Conclusions: Long-term exposure to particulate matter was associated with small increases in risk of incident hypertension, particularly among younger women and the obese.
Citation: Zhang Z, Laden F, Forman JP, Hart JE. 2016. Long-term exposure to particulate matter and self-reported hypertension: a prospective analysis in the Nurses’ Health Study. Environ Health Perspect 124:1414–1420; http://dx.doi.org/10.1289/EHP163
Background: Survivors of acute myocardial infarction (AMI) are at increased risk of dying within several hours to days following exposure to elevated levels of ambient air pollution. Little is known, however, about the influence of long-term (months to years) air pollution exposure on survival after AMI.
Objective: We conducted a population-based cohort study to determine the impact of long-term exposure to fine particulate matter ≤ 2.5 μm in diameter (PM2.5) on post-AMI survival.
Methods: We assembled a cohort of 8,873 AMI patients who were admitted to 1 of 86 hospital corporations across Ontario, Canada in 1999–2001. Mortality follow-up for this cohort extended through 2011. Cumulative time-weighted exposures to PM2.5 were derived from satellite observations based on participants’ annual residences during follow-up. We used standard and multilevel spatial random-effects Cox proportional hazards models and adjusted for potential confounders.
Results: Between 1999 and 2011, we identified 4,016 nonaccidental deaths, of which 2,147 were from any cardiovascular disease, 1,650 from ischemic heart disease, and 675 from AMI. For each 10-μg/m3 increase in PM2.5, the adjusted hazard ratio (HR10) of nonaccidental mortality was 1.22 [95% confidence interval (CI): 1.03, 1.45]. The association with PM2.5 was robust to sensitivity analyses and appeared stronger for cardiovascular-related mortality: ischemic heart (HR10 = 1.43; 95% CI: 1.12, 1.83) and AMI (HR10 = 1.64; 95% CI: 1.13, 2.40). We estimated that 12.4% of nonaccidental deaths (or 497 deaths) could have been averted if the lowest measured concentration in an urban area (4 μg/m3) had been achieved at all locations over the course of the study.
Conclusions: Long-term air pollution exposure adversely affects the survival of AMI patients.
Citation: Chen H, Burnett RT, Copes R, Kwong JC, Villeneuve PJ, Goldberg MS, Brook RD, van Donkelaar A, Jerrett M, Martin RV, Brook JR, Kopp A, Tu JV. 2016. Ambient fine particulate matter and mortality among survivors of myocardial infarction: population-based cohort study. Environ Health Perspect 124:1421–1428; http://dx.doi.org/10.1289/EHP185
Background: Psychological sequelae are among the most pronounced effects in populations following exposure to oil spills. Women in particular represent a vulnerable yet influential population but have remained relatively understudied with respect to the Deepwater Horizon oil spill (DHOS).
Objective: To describe the relationship between oil spill exposure and mental health among women living in the southern coastal Louisiana parishes affected by the DHOS.
Methods: The Women and Their Children’s Health Study administered telephone interviews to a population-based sample of 2,842 women between 2012 and 2014 following the DHOS. Participants were asked about depression, mental distress, domestic conflict, and exposure to the oil spill.
Results: Over 28% of the sample reported symptoms of depression, 13% reported severe mental distress, 16% reported an increase in the number of fights with their partners, and 11% reported an increase in the intensity of partner fights. Both economic and physical exposure were significantly associated with depressive symptoms and domestic conflict, whereas only physical exposure was related to mental distress.
Conclusions: This large, population-based study of women in southern coastal Louisiana, a particularly disaster-prone area of the country, revealed high rates of poor mental health outcomes. Reported exposure to the DHOS was a significant predictor of these outcomes, suggesting avenues for future disaster mitigation through the provision of mental health services.
Citation: Rung AL, Gaston S, Oral E, Robinson WT, Fontham E, Harrington DJ, Trapido E, Peters ES. 2016. Depression, mental distress, and domestic conflict among Louisiana women exposed to the Deepwater Horizon Oil Spill in the WaTCH Study. Environ Health Perspect 124:1429–1435; http://dx.doi.org/10.1289/EHP167
Background: Although occupational exposures contribute to a significant proportion of obstructive lung disease, the phenotype of obstructive lung disease associated with work-related organic dust exposure independent of smoking remains poorly defined.
Objective: We identified the relative contributions of smoking and occupational endotoxin exposure to parenchymal and airway remodeling as defined by quantitative computed tomography (CT).
Methods: The Shanghai Textile Worker Study is a longitudinal study of endotoxin-exposed cotton workers and endotoxin-unexposed silk workers that was initiated in 1981. Spirometry, occupational endotoxin exposure, and smoking habits were assessed at 5-year intervals. High-resolution computed tomography (CT) was performed in 464 retired workers in 2011, along with quantitative lung densitometric and airway analysis.
Results: Significant differences in all CT measures were noted across exposure groups. Occupational endotoxin exposure was associated with a decrease (–1.3%) in percent emphysema (LAAI-950), a 3.3-Hounsfield unit increase in 15th percentile density, an 18.1-g increase in lung mass, and a 2.3% increase in wall area percent. Current but not former smoking was associated with a similar CT phenotype. Changes in LAAI-950 were highly correlated with 15th percentile density (correlation –1.0). Lung mass was the only measure associated with forced expiratory volume in 1 sec (FEV1) decline, with each 10-g increase in lung mass associated with an additional loss (–6.1 mL) of FEV1 (p = 0.001) between 1981 and 2011.
Conclusions: There are many similarities between the effects of occupational endotoxin exposure and those of tobacco smoke exposure on lung parenchyma and airway remodeling. The effects of occupational endotoxin exposure appear to persist even after the cessation of exposure. LAAI-950 may not be a reliable indicator of emphysema in subjects without spirometric impairment. Lung mass is a CT-based biomarker of accelerated lung function decline.
Citation: Lai PS, Hang J, Zhang F, Sun J, Zheng BY, Su L, Washko GR, Christiani DC. 2016. Imaging phenotype of occupational endotoxin-related lung function decline. Environ Health Perspect 124:1436–1442; http://dx.doi.org/10.1289/EHP195
Background: Ambient monitoring data show spatial gradients in ozone (O3) across urban areas. Nitrogen oxide (NOx) emissions reductions will likely alter these gradients. Epidemiological studies often use exposure surrogates that may not fully account for the impacts of spatially and temporally changing concentrations on population exposure.
Objectives: We examined the impact of large NOx decreases on spatial and temporal O3 patterns and the implications on exposure.
Methods: We used a photochemical model to estimate O3 response to large NOx reductions. We derived time series of 2006–2008 O3 concentrations consistent with 50% and 75% NOx emissions reduction scenarios in three urban areas (Atlanta, Philadelphia, and Chicago) at each monitor location and spatially interpolated O3 to census-tract centroids.
Results: We predicted that low O3 concentrations would increase and high O3 concentrations would decrease in response to NOx reductions within an urban area. O3 increases occurred across larger areas for the seasonal mean metric than for the regulatory metric (annual 4th highest daily 8-hr maximum) and were located only in urban core areas. O3 always decreased outside the urban core (e.g., at locations of maximum local ozone concentration) for both metrics and decreased within the urban core in some instances. NOx reductions led to more uniform spatial gradients and diurnal and seasonal patterns and caused seasonal peaks in midrange O3 concentrations to shift from midsummer to earlier in the year.
Conclusions: These changes have implications for how O3 exposure may change in response to NOx reductions and are informative for the design of future epidemiology studies and risk assessments.
Citation: Simon H, Wells B, Baker KR, Hubbell B. 2016. Assessing temporal and spatial patterns of observed and predicted ozone in multiple urban areas. Environ Health Perspect 124:1443–1452; http://dx.doi.org/10.1289/EHP190
Background: Integrative testing strategies (ITSs) for potential endocrine activity can use tiered in silico and in vitro models. Each component of an ITS should be thoroughly assessed.
Objectives: We used the data from three in vitro ToxCast™ binding assays to assess OASIS, a quantitative structure-activity relationship (QSAR) platform covering both estrogen receptor (ER) and androgen receptor (AR) binding. For stronger binders (described here as AC50 < 1 μM), we also examined the relationship of QSAR predictions of ER or AR binding to the results from 18 ER and 10 AR transactivation assays, 72 ER-binding reference compounds, and the in vivo uterotrophic assay.
Methods: NovaScreen binding assay data for ER (human, bovine, and mouse) and AR (human, chimpanzee, and rat) were used to assess the sensitivity, specificity, concordance, and applicability domain of two OASIS QSAR models. The binding strength relative to the QSAR-predicted binding strength was examined for the ER data. The relationship of QSAR predictions of binding to transactivation- and pathway-based assays, as well as to in vivo uterotrophic responses, was examined.
Results: The QSAR models had both high sensitivity (> 75%) and specificity (> 86%) for ER as well as both high sensitivity (92–100%) and specificity (70–81%) for AR. For compounds within the domains of the ER and AR QSAR models that bound with AC50 < 1 μM, the QSAR models accurately predicted the binding for the parent compounds. The parent compounds were active in all transactivation assays where metabolism was incorporated and, except for those compounds known to require metabolism to manifest activity, all assay platforms where metabolism was not incorporated. Compounds in-domain and predicted to bind by the ER QSAR model that were positive in ToxCast™ ER binding at AC50 < 1 μM were active in the uterotrophic assay.
Conclusions: We used the extensive ToxCast™ HTS binding data set to show that OASIS ER and AR QSAR models had high sensitivity and specificity when compounds were in-domain of the models. Based on this research, we recommend a tiered screening approach wherein a) QSAR is used to identify compounds in-domain of the ER or AR binding models and predicted to bind; b) those compounds are screened in vitro to assess binding potency; and c) the stronger binders (AC50 < 1 μM) are screened in vivo. This scheme prioritizes compounds for integrative testing and risk assessment. Importantly, compounds that are not in-domain, that are predicted either not to bind or to bind weakly, that are not active in in vitro, that require metabolism to manifest activity, or for which in vivo AR testing is in order, need to be assessed differently.
Citation: Bhhatarai B, Wilson DM, Price PS, Marty S, Parks AK, Carney E. 2016. Evaluation of OASIS QSAR models using ToxCast™ in vitro estrogen and androgen receptor binding data and application in an integrated endocrine screening approach. Environ Health Perspect 124:1453–1461; http://dx.doi.org/10.1289/EHP184
Background: Soil/dust ingestion rates are important variables in assessing children’s health risks in contaminated environments. Current estimates are based largely on soil tracer methodology, which is limited by analytical uncertainty, small sample size, and short study duration.
Objectives: The objective was to estimate site-specific soil/dust ingestion rates through reevaluation of the lead absorption dose–response relationship using new bioavailability data from the Bunker Hill Mining and Metallurgical Complex Superfund Site (BHSS) in Idaho, USA.
Methods: The U.S. Environmental Protection Agency (EPA) in vitro bioavailability methodology was applied to archived BHSS soil and dust samples. Using age-specific biokinetic slope factors, we related bioavailable lead from these sources to children’s blood lead levels (BLLs) monitored during cleanup from 1988 through 2002. Quantitative regression analyses and exposure assessment guidance were used to develop candidate soil/dust source partition scenarios estimating lead intake, allowing estimation of age-specific soil/dust ingestion rates. These ingestion rate and bioavailability estimates were simultaneously applied to the U.S. EPA Integrated Exposure Uptake Biokinetic Model for Lead in Children to determine those combinations best approximating observed BLLs.
Results: Absolute soil and house dust bioavailability averaged 33% (SD ± 4%) and 28% (SD ± 6%), respectively. Estimated BHSS age-specific soil/dust ingestion rates are 86–94 mg/day for 6-month- to 2-year-old children and 51–67 mg/day for 2- to 9-year-old children.
Conclusions: Soil/dust ingestion rate estimates for 1- to 9-year-old children at the BHSS are lower than those commonly used in human health risk assessment. A substantial component of children’s exposure comes from sources beyond the immediate home environment.
Citation: von Lindern I, Spalinger S, Stifelman ML, Stanek LW, Bartrem C. 2016. Estimating children’s soil/dust ingestion rates through retrospective analyses of blood lead biomonitoring from the Bunker Hill Superfund Site in Idaho. Environ Health Perspect 124:1462–1470; http://dx.doi.org/10.1289/ehp.1510144
Background: From 2010 through 2013, integrated health and environmental responses addressed an unprecedented epidemic lead poisoning in Zamfara State, northern Nigeria. Artisanal gold mining caused widespread contamination resulting in the deaths of > 400 children. Socioeconomic, logistic, and security challenges required remediation and medical protocols within the context of local resources, labor practices, and cultural traditions.
Objectives: Our aim was to implement emergency environmental remediation to abate exposures to 17,000 lead poisoned villagers, to facilitate chelation treatment of children ≤ 5 years old, and to establish local technical capacity and lead health advocacy programs to prevent future disasters.
Methods: U.S. hazardous waste removal protocols were modified to accommodate local agricultural practices. Remediation was conducted over 4 years in three phases, progressing from an emergency response by international personnel to comprehensive cleanup funded and accomplished by the Nigerian government.
Results: More than 27,000 m3 of contaminated soils and mining waste were removed from 820 residences and ore processing areas in eight villages, largely by hand labor, and disposed in constructed landfills. Excavated areas were capped with clean soils (≤ 25 mg/kg lead), decreasing soil lead concentrations by 89%, and 2,349 children received chelation treatment. Pre-chelation geometric mean blood lead levels for children ≤ 5 years old decreased from 149 μg/dL to 15 μg/dL over the 4-year remedial program.
Conclusions: The unprecedented outbreak and response demonstrate that, given sufficient political will and modest investment, the world’s most challenging environmental health crises can be addressed by adapting proven response protocols to the capabilities of host countries.
Citation: Tirima S, Bartrem C, von Lindern I, von Braun M, Lind D, Anka SM, Abdullahi A. 2016. Environmental remediation to address childhood lead poisoning epidemic due to artisanal gold mining in Zamfara, Nigeria. Environ Health Perspect 124:1471–1478; http://dx.doi.org/10.1289/ehp.1510145
Background: Preterm birth (PTB) has been associated with exposure to air pollution, but it is unclear whether effects might vary among air pollution sources and components.
Objectives: We studied the relationships between PTB and exposure to different components of air pollution, including gases and particulate matter (PM) by size fraction, chemical composition, and sources.
Methods: Fine and ultrafine PM (respectively, PM2.5 and PM0.1) by source and composition were modeled across California over 2000–2008. Measured PM2.5, nitrogen dioxide, and ozone concentrations were spatially interpolated using empirical Bayesian kriging. Primary traffic emissions at fine scale were modeled using CALINE4 and traffic indices. Data on maternal characteristics, pregnancies, and birth outcomes were obtained from birth certificates. Associations between PTB (n = 442,314) and air pollution exposures defined according to the maternal residence at birth were examined using a nested matched case–control approach. Analyses were adjusted for maternal age, race/ethnicity, education and neighborhood income.
Results: Adjusted odds ratios for PTB in association with interquartile range (IQR) increases in average exposure during pregnancy were 1.133 (95% CI: 1.118, 1.148) for total PM2.5, 1.096 (95% CI: 1.085, 1.108) for ozone, and 1.079 (95% CI: 1.065, 1.093) for nitrogen dioxide. For primary PM, the strongest associations per IQR by source were estimated for onroad gasoline (9–11% increase), followed by onroad diesel (6–8%) and commercial meat cooking (4–7%). For PM2.5 composition, the strongest positive associations per IQR were estimated for nitrate, ammonium, and secondary organic aerosols (11–14%), followed by elemental and organic carbon (2–4%). Associations with local traffic emissions were positive only when analyses were restricted to births with residences geocoded at the tax parcel level.
Conclusions: In our statewide nested case–control study population, exposures to both primary and secondary pollutants were associated with an increase in PTB.
Citation: Laurent O, Hu J, Li L, Kleeman MJ, Bartell SM, Cockburn M, Escobedo L, Wu J. 2016. A statewide nested case–control study of preterm birth and air pollution by source and composition: California, 2001–2008. Environ Health Perspect 124:1479–1486; http://dx.doi.org/10.1289/ehp.1510133
Background: Incense burning for rituals or religious purposes is an important tradition in many countries. However, incense smoke contains particulate matter and gas products such as carbon monoxide, sulfur, and nitrogen dioxide, which are potentially harmful to health.
Objectives: We analyzed the relationship between prenatal incense burning and birth weight and head circumference at birth using the Taiwan Birth Cohort Study. We also analyzed whether the associations varied by sex and along the distribution of birth outcomes.
Methods: We performed ordinary least squares (OLS) and quantile regressions analysis on a sample of 15,773 term births (> 37 gestational weeks; 8,216 boys and 7,557 girls) in Taiwan in 2005. The associations were estimated separately for boys and girls as well as for the population as a whole. We controlled extensively for factors that may be correlated with incense burning and birth weight and head circumference, such as parental religion, demographics, and health characteristics, as well as pregnancy-related variables.
Results: Findings from fully adjusted OLS regressions indicated that exposure to incense was associated with lower birth weight in boys (–18 g; 95% CI: –36, –0.94) but not girls (1 g; 95% CI: –17, 19; interaction p-value = 0.31). Associations with head circumference were negative for boys (–0.95 mm; 95% CI: –1.8, –0.16) and girls (–0.71 mm; 95% CI: –1.5, 0.11; interaction p-values = 0.73). Quantile regression results suggested that the negative associations were larger among the lower quantiles of birth outcomes.
Conclusions: OLS regressions showed that prenatal incense burning was associated with lower birth weight for boys and smaller head circumference for boys and girls. The associations were more pronounced among the lower quantiles of birth outcomes. Further research is necessary to confirm whether incense burning has differential effects by sex.
Citation: Chen LY, Ho C. 2016. Incense burning during pregnancy and birth weight and head circumference among term births: The Taiwan Birth Cohort Study. Environ Health Perspect 124:1487–1492; http://dx.doi.org/10.1289/ehp.1509922
For nearly 30 years, Dr. Theo Colborn (1927–2014) dedicated herself to studying the harmful effects of endocrine-disrupting chemicals on wildlife, humans, and the environment. More recently, she extended this effort to address the health impacts of unconventional oil and gas development. Colborn was a visionary leader who excelled at synthesizing scientific findings across disciplines. Using her unique insights and strong moral convictions, she changed the face of toxicological research, influenced chemical regulatory policy, and educated the public. In 2003, Colborn started a nonprofit organization—The Endocrine Disruption Exchange (TEDX). As we celebrate the 25th anniversary of endocrine disruption science, TEDX continues her legacy of analyzing the extensive body of environmental health research and developing unique educational resources to support public policy and education. Among other tools, TEDX currently uses the systematic review framework developed by the National Toxicology Program at the National Institute of Environmental Health Sciences, to answer research questions of pressing concern. In this article, we pay homage to the tenacious woman and the exemplary contribution she made to the field of environmental health. Recommendations for the future of the field are drawn from her wisdom.