Showing papers in "Environmental Health Perspectives in 2011"
TL;DR: PD was positively associated with two groups of pesticides defined by mechanisms implicated experimentally—those that impair mitochondrial function and those that increase oxidative stress—supporting a role for these mechanisms in PD pathophysiology.
Abstract: BackgroundMitochondrial dysfunction and oxidative stress are pathophysiologic mechanisms implicated in experimental models and genetic forms of Parkinson’s disease (PD). Certain pesticides may affe...
1,151 citations
TL;DR: In this article, the authors compared the potential health benefits of a hypothetical traffic abatement measure, using near-roadway concentration increments of BCP and PM2.5 based on data from prior studies.
Abstract: Background: Current air quality standards for particulate matter (PM) use the PM mass concentration [PM with aerodynamic diameters ≤ 10 μm (PM10) or ≤ 2.5 μm (PM2.5)] as a metric. It has been suggested that particles from combustion sources are more relevant to human health than are particles from other sources, but the impact of policies directed at reducing PM from combustion processes is usually relatively small when effects are estimated for a reduction in the total mass concentration.
Objectives: We evaluated the value of black carbon particles (BCP) as an additional indicator in air quality management.
Methods: We performed a systematic review and meta-analysis of health effects of BCP compared with PM mass based on data from time-series studies and cohort studies that measured both exposures. We compared the potential health benefits of a hypothetical traffic abatement measure, using near-roadway concentration increments of BCP and PM2.5 based on data from prior studies.
Results: Estimated health effects of a 1-μg/m3 increase in exposure were greater for BCP than for PM10 or PM2.5, but estimated effects of an interquartile range increase were similar. Two-pollutant models in time-series studies suggested that the effect of BCP was more robust than the effect of PM mass. The estimated increase in life expectancy associated with a hypothetical traffic abatement measure was four to nine times higher when expressed in BCP compared with an equivalent change in PM2.5 mass.
Conclusion: BCP is a valuable additional air quality indicator to evaluate the health risks of air quality dominated by primary combustion particles.
859 citations
TL;DR: Biomonitoring data from the National Health and Nutritional Examination Survey (NHANES) found that levels in pregnant women were similar to or lower than levels in nonpregnant women; adjustment for covariates tended to increase levels innant women compared with nonpRegnant women.
Abstract: BackgroundExposure to chemicals during fetal development can increase the risk of adverse health effects, and while biomonitoring studies suggest pregnant women are exposed to chemicals, little is ...
758 citations
TL;DR: Prevention and remediation of indoor dampness and mold are likely to reduce health risks, but current evidence does not support measuring specific indoor microbiologic factors to guide health-protective actions.
Abstract: ObjectivesMany studies have shown consistent associations between evident indoor dampness or mold and respiratory or allergic health effects, but causal links remain unclear. Findings on measured m...
749 citations
TL;DR: At low exposure levels, cardiovascular deaths are projected to account for most of the burden of disease, whereas at high levels of PM2.5, lung cancer becomes proportionately more important.
Abstract: Background: Lung cancer and cardiovascular disease (CVD) mortality risks increase with smoking, secondhand smoke (SHS), and exposure to fine particulate matter < 2.5 μm in diameter (PM2.5) from amb...
623 citations
TL;DR: Prenatal but not postnatal urinary DAP concentrations were associated with poorer intellectual development in 7-year-old children, higher but nonetheless within the range of levels measured in the general U.S. population.
Abstract: Context: Organophosphate (OP) pesticides are neurotoxic at high doses. Few studies have examined whether chronic exposure at lower levels could adversely impact children’s cognitive development.
Objective: To examine associations between prenatal and postnatal exposure to OP pesticides and cognitive abilities in school-age children.
Methods: We conducted a birth-cohort study (CHAMACOS) among predominantly Latino farmworker families from an agricultural community in California. We assessed exposure to OP pesticides by measuring dialkyl phosphate (DAP) metabolites in urine collected during pregnancy and from children at age 6 months and 1, 2, 3½ and 5 years. We administered the Wechsler Intelligence Scale for Children-IV to 329 seven-year old children. Analyses were adjusted for maternal education and intelligence, HOME score, and language of cognitive assessment.
Results: Urinary DAP concentrations measured during the 1st and 2nd half of pregnancy had similar relations to cognitive scores, thus we used the average of concentrations measured during pregnancy in further analyses. Averaged maternal DAP concentrations were associated with poorer scores for Working Memory, Processing Speed, Verbal Comprehension, Perceptual Reasoning, and Full Scale IQ. Children in the highest quintile of maternal DAP concentrations had an average deficit of 7.0 IQ-points compared with those in the lowest quintile. However, children’s urinary DAP concentrations were not consistently associated with cognitive scores.
Conclusions: Prenatal but not postnatal urinary DAP concentrations were associated with poorer intellectual development in 7-year-old children. Maternal urinary DAP concentrations in the present study were higher, but nonetheless within the range of levels measured in the general U.S. population.
545 citations
TL;DR: BPA and DEHP exposures were substantially reduced when participants’ diets were restricted to food with limited packaging and change in urinary levels across time was assessed.
Abstract: Background: Bisphenol A (BPA) and bis(2-ethylhexyl) phthalate (DEHP) are high-production-volume chemicals used in plastics and resins for food packaging. They have been associated with endocrine di...
470 citations
TL;DR: Evidence of deficits in Working Memory Index and Full-Scale IQ as a function of prenatal CPF exposure at 7 years of age is reported, important in light of continued widespread use of CPF in agricultural settings and possible longer-term educational implications of early cognitive deficits.
Abstract: Background: In a longitudinal birth cohort study of inner-city mothers and children (Columbia Center for Children’s Environmental Health), we have previously reported that prenatal exposure to chlo...
439 citations
TL;DR: The scientific evidence for the seasonal mechanisms that potentially explain the complex seasonal patterns of influenza disease activity observed globally is examined and an analytical framework is developed that highlights the complex interactions among environmental stimuli, mediating mechanisms, and the seasonal timing of influenza epidemics.
Abstract: BACKGROUND: Despite the significant disease burden of the influenza virus in humans, our understanding of the basis for its pronounced seasonality remains incomplete. Past observations that influenza epidemics occur in the winter across temperate climates, combined with insufficient knowledge about the epidemiology of influenza in the tropics, led to the perception that cool and dry conditions were a necessary, and possibly sufficient, driver of influenza epidemics. Recent reports of substantial levels of influenza virus activity and well-defined seasonality in tropical regions, where warm and humid conditions often persist year-round, have rendered previous hypotheses insufficient for explaining global patterns of influenza. OBJECTIVE: In this review, we examined the scientific evidence for the seasonal mechanisms that potentially explain the complex seasonal patterns of influenza disease activity observed globally. METHODS: In this review we assessed the strength of a range of hypotheses that attempt to explain observations of influenza seasonality across different latitudes and how they relate to each other. We reviewed studies describing population-scale observations, mathematical models, and ecological, laboratory, and clinical experiments pertaining to influenza seasonality. The literature review includes studies that directly mention the topic of influenza seasonality, as well as other topics we believed to be relevant. We also developed an analytical framework that highlights the complex interactions among environmental stimuli, mediating mechanisms, and the seasonal timing of influenza epidemics and identify critical areas for further research. CONCLUSIONS: The central questions in influenza seasonality remain unresolved. Future research is particularly needed in tropical localities, where our understanding of seasonality remains poor, and will require a combination of experimental and observational studies. Further understanding of the environmental factors that drive influenza circulation also may be useful to predict how dynamics will be affected at regional levels by global climate change.
414 citations
TL;DR: Evidence of an inverse association of 2,5-DCP and a positive association of BP3 with male birth weight is observed and there was no evidence of monotonic associations with birth weight.
Abstract: Background: Data concerning the effects of prenatal exposures to phthalates and phenols on fetal growth are limited in humans. Previous findings suggest possible effects of some phenols on male bir...
400 citations
TL;DR: In this article, the authors used a case-crossover design to examine nonlinear and distributed lag effects of temperature on mortality in Tianjin, China and explore which temperature measure is the best predictor of mortality.
Abstract: Background : Although interest in assessing the impacts of temperature on mortality has increased, few studies have used a case-crossover design to examine non linear and distributed lag effects of temperature on mortality. Additionally, little evidence is available on the temperature–mortality relationship in China or on what temperature measure is the best predictor of mortality. oB jectives : Our objectives were to use a distributed lag nonlinear model (DLNM) as a part of casecrossover design to examine the nonlinear and distributed lag effects of temperature on mortality in Tianjin, China and to explore which temperature measure is the best predictor of mortality. Methods : We applied the DLNM to a case-crossover design to assess the nonlinear and delayed effects of temperatures (maximum, mean , and minimum) on deaths (nonaccidental, cardiopulmonary, cardiovascular, and respiratory). results : A U-shaped relationship was found consistently between temperature and mortality. Cold effects (i.e., significantly increased mortality associated with low temperatures) were delayed by 3 days and persisted for 10 days. Hot effects (i.e., significantly increased mortality associated with high temperatures) were acute and lasted for 3 days and were followed by mortality displacement for nonaccidental, cardiopulmonary, and cardiovascular deaths. Mean temperature was a better predictor of mortality (based on model fit) than maximum or minimum temperature. conclusions : In Tianjin, extreme cold and hot temperatures increased the risk of mortality. The effects of cold last longer than the effects of heat. Combining the DLNM and the case-crossover design allows the case-crossover design to flexibly estimate the nonlinear and delayed effects of temperature (or air pollution) while controlling for season.
TL;DR: The existing evidence on thirdhand smoke (THS) provides strong support for pursuing a programmatic research agenda to close gaps in current understanding of the chemistry, exposure, toxicology, and health effects of THS, as well as its behavioral, economic, and sociocultural considerations and consequences.
Abstract: Background: There is broad consensus regarding the health impact of tobacco use and secondhand smoke exposure, yet considerable ambiguity exists about the nature and consequences of thirdhand smoke (THS).
Objectives: We introduce definitions of THS and THS exposure and review recent findings about constituents, indoor sorption–desorption dynamics, and transformations of THS; distribution and persistence of THS in residential settings; implications for pathways of exposure; potential clinical significance and health effects; and behavioral and policy issues that affect and are affected by THS.
Discussion: Physical and chemical transformations of tobacco smoke pollutants take place over time scales ranging from seconds to months and include the creation of secondary pollutants that in some cases are more toxic (e.g., tobacco-specific nitrosamines). THS persists in real-world residential settings in the air, dust, and surfaces and is associated with elevated levels of nicotine on hands and cotinine in urine of nonsmokers residing in homes previously occupied by smokers. Much still needs to be learned about the chemistry, exposure, toxicology, health risks, and policy implications of THS.
Conclusion: The existing evidence on THS provides strong support for pursuing a programmatic research agenda to close gaps in our current understanding of the chemistry, exposure, toxicology, and health effects of THS, as well as its behavioral, economic, and sociocultural considerations and consequences. Such a research agenda is necessary to illuminate the role of THS in existing and future tobacco control efforts to decrease smoking initiation and smoking levels, to increase cessation attempts and sustained cessation, and to reduce the cumulative effects of tobacco use on morbidity and mortality.
TL;DR: The Hidden Costs of Energy, which provides quantitative, qualitative, and in some cases monetized estimates of these external damages from the use of energy for electricity, transportation, heat, and infrastructure and security, is produced.
Abstract: The production and consumption of energy and its derived services have raised the living standards of billions. Energy is traded in markets, and its price in most cases does not reflect the full cost of its use to society. Absent regulation, only the private cost of producing, for example, a kilowatt hour (kWh) of electricity is paid for by consumers through their electricity bills. These private costs, however, fail to account for a variety of external costs from this production activity in the form of, for example, present-day health damages from increased air pollution or potentially lower grain yields due to global warming halfway around the world and almost a century into the future. Economists argue that regulators should make producers “internalize” the external costs, preferably through flexible market mechanisms such as pollution taxes or cap-and-trade systems. Although qualitatively this can be easily explained to an undergraduate student in a 45-minute lecture, the exact magnitude of the full external costs is impossible to determine. The difficulty in determining the damages is caused by the significant degree of uncertainty in our understanding of the source-to-dose relationship combined with an even more limited understanding of the dose–response relationships for the vast variety of pollutants and potentially affected populations and systems. Monetizing the damages (and, in rare cases, benefits) is further complicated by the fact that many affected “receptors” of the pollution are not traded in markets and therefore do not carry a price.
The National Academy of Sciences was charged by Congress to “define and evaluate the health, environmental, security, and infrastructural external costs and benefits that are not or may not be fully incorporated into the market price of energy [or] into the federal tax or fee.” The National Research Council committee, convened for this purpose and chaired by Jared Cohon and vice-chaired by Maureen Cropper, produced the report Hidden Costs of Energy, which provides quantitative, qualitative, and in some cases monetized estimates of these external damages from the use of energy for electricity, transportation, heat, and infrastructure and security.
The central estimate of damages, which has been widely reported in the press, of US$120 billion for the last year of available data (2005) must be interpreted as a strict lower bound of the true external costs. Fifty-two percent of the estimated damages arises from health-related damages from the combustion of coal for electricity; 47% stems from the combustion of liquid fuels for transport. The remaining US$2 billion in damages are attributable to health effects from natural gas for electricity production and heating. To put this in perspective, the average price per kilowatt hour of electricity in the United States is approximately 10 cents—slightly higher for residential customers and slightly lower for industrial customers. The health damages from coal alone are 3.2 cents/kWh, with some plants having external costs at 12 cents/kWh.
The book does not include the damages from climate change in its total costs, yet provides an intriguing calculation. If one assumed marginal damages to be $30/ton of carbon dioxide, the external costs from climate change per kilowatt hour are also in the neighborhood of 3 cents—doubling the estimated external costs.
Two other factors that will drive up the true external costs of energy are the impacts on ecosystems and the impacts on national security—either of which are extremely difficult to value. For health damages, the report uses the value of a statistical (human) life of US$6 million, which is based on a large universe of existing willingness-to-pay studies. With the dearth of such studies in the heterogeneous ecosystem context, one cannot credibly and comprehensively determine what the overall monetary damages on ecosystems are.
Even though a number of important effects have not been monetized, this report is the essential work in this area and belongs in the library of any serious researcher, policy maker, or writer working in this area. It is the most serious yet accessible assessment and literature review available of the external life-cycle costs of the energy system for the U.S. economy.
TL;DR: It is suggested that prenatal exposure to organophosphates is negatively associated with cognitive development, particularly perceptual reasoning, with evidence of effects beginning at 12 months and continuing through early childhood.
Abstract: Background: Prenatal exposure to organophosphate pesticides has been shown to negatively impact child neurobehavioral development. Paraoxonase 1 (PON1) is a key enzyme in the metabolism of organophosphates.
Objective: To examine the relationship between biomarkers of organophosphate exposure, PON1, and cognitive development at ages 12 and 24 months, and 6 to 9 years.
Methods: The Mount Sinai Children’s Environmental Health Study enrolled a multiethnic prenatal population in New York City between 1998 and 2002 (n= 404). Third trimester maternal urines were collected and analyzed for organophosphate metabolites (n = 360). Prenatal maternal blood was analyzed for PON1 activity and genotype. Children returned for neurodevelopment assessments at ages 12 months (n = 200), 24 months (n = 276), 6 to 9 (n = 169) years.
Results: Prenatal total dialkylphosphate metabolite level was associated with a decrement in mental development at 12 months among blacks and Hispanics. These associations appeared to be enhanced among children of mothers who carried the PON1 Q192R QQ genotype, which imparts slow catalytic activity for chlorpyrifos oxon. In later childhood, increasing prenatal total dialkyl- and dimethylphosphate metabolites were associated with decrements in perceptual reasoning in the maternal PON1 Q192R QQ genotype, with a monotonic trend consistent with greater decrements with increasing prenatal exposure.
Conclusion: Our findings suggest that prenatal exposure to organophosphates negatively impacts cognitive development, particularly perceptual reasoning, with evidence of effects beginning at 12 months and continuing through early childhood. PON1 may be an important susceptibility factor for these deleterious effects.
TL;DR: The results support the influence of night temperatures on the health impact of heat waves in urban areas and have the potential to identify areas with higher risk of death, which could inform intervention decisions by key stakeholders.
Abstract: Background: Heat waves have a drastic impact on urban populations, which could increase with climate change.
Objectives: We evaluated new indicators of elderly people’s exposure to heat in Paris, from a public health prevention perspective, using satellite thermal images.
Methods: We used a time series of 61 images from the satellites of the National Oceanic and Atmospheric Administration’s (NOAA) Advanced Very High Resolution Radiometer (AVHRR) taken from 1 to 13 August 2003 to produce thermal indicators of minimum, maximum, and mean surface temperatures and diurnal temperature amplitude, with different lags between the meteorological data and the health impact. Health data came from a case–control study involving 241 people ≥ 65 years of age who died in the city of Paris or the nearby suburban area of Val-de-Marne during the August 2003 heat wave, and 241 controls who were matched to cases on age, sex, and residential zone. For each person, we integrated the thermal indicators in a conditional logistic regression model, adjusted for age and other potential confounders. We computed odds ratios (ORs) comparing the 90th and 50th percentiles of the temperature differences between cases and controls for various indicators.
Results: Mortality risk was significantly associated with exposure for two indicators: minimum temperatures averaged for 1–13 August [for a 0.41°C increase, OR = 2.17; 95% confidence interval (CI): 1.14, 4.16] and minimum temperature averaged on the day of death and the 6 preceding days (for a 0.51°C increase: OR = 2.24; 95% CI: 1.03, 4.87).
Conclusions: Our results support the influence of night temperatures on the health impact of heat waves in urban areas. Urban heat exposure indicators based on satellite imagery have the potential to identify areas with higher risk of death, which could inform intervention decisions by key stakeholders.
TL;DR: In this article, a systematic review of research and methods for projecting future heat-related mortality under climate change scenarios was conducted. But, the authors did not consider the potential impacts of climate change on heat related mortality.
Abstract: Background: Heat-related mortality is a matter of great public health concern, especially in the light of climate change. Although many studies have found associations between high temperatures and mortality, more research is needed to project the future impacts of climate change on heat-related mortality.
Objectives: We conducted a systematic review of research and methods for projecting future heat-related mortality under climate change scenarios.
Data sources and extraction: A literature search was conducted in August 2010, using the electronic databases PubMed, Scopus, ScienceDirect, ProQuest, and Web of Science. The search was limited to peer-reviewed journal articles published in English from January 1980 through July 2010.
Data synthesis: Fourteen studies fulfilled the inclusion criteria. Most projections showed that climate change would result in a substantial increase in heat-related mortality. Projecting heat-related mortality requires understanding historical temperature–mortality relationships and considering the future changes in climate, population, and acclimatization. Further research is needed to provide a stronger theoretical framework for projections, including a better understanding of socioeconomic development, adaptation strategies, land-use patterns, air pollution, and mortality displacement.
Conclusions: Scenario-based projection research will meaningfully contribute to assessing and managing the potential impacts of climate change on heat-related mortality.
TL;DR: The evidence supporting the roles of the three major epigenetic mechanisms—DNA methylation, histone modification, and microRNA (miRNA) expression—in arsenic toxicity and, in particular, carcinogenicity was examined.
Abstract: BackgroundExposure to arsenic, an established human carcinogen, through consumption of highly contaminated drinking water is a worldwide public health concern. Several mechanisms by which arsenical...
TL;DR: The data suggest that EA-free plastic products exposed to common-use stresses and extracted by saline and ethanol solvents could be cost-effectively made on a commercial scale and thereby eliminate a potential health risk posed by most currently available plastic products that leach chemicals having EA into food products.
Abstract: This work was supported by National Institutes
of Health (NIH) grants R44 ES011469 (01-03)
and 1R43/44 ES014806 (01-03) to C.Z.Y.; R44
ES016964 (01-03) to S.I.Y.; and P30 CA051008
to V.C.J.
TL;DR: Together, these findings reveal complex, interacting mechanisms responsible for how air pollution may cause neuroinflammation and DA neurotoxicity.
Abstract: Background: Air pollution is linked to central nervous system disease, but the mechanisms responsible are poorly understood.
Objectives: Here, we sought to address the brain-region–specific effects of diesel exhaust (DE) and key cellular mechanisms underlying DE-induced microglia activation, neuroinflammation, and dopaminergic (DA) neurotoxicity.
Methods: Rats were exposed to DE (2.0, 0.5, and 0 mg/m3) by inhalation over 4 weeks or as a single intratracheal administration of DE particles (DEP; 20 mg/kg). Primary neuron–glia cultures and the HAPI (highly aggressively proliferating immortalized) microglial cell line were used to explore cellular mechanisms.
Results: Rats exposed to DE by inhalation demonstrated elevated levels of whole-brain IL-6 (interleukin-6) protein, nitrated proteins, and IBA-1 (ionized calcium-binding adaptor molecule 1) protein (microglial marker), indicating generalized neuroinflammation. Analysis by brain region revealed that DE increased TNFα (tumor necrosis factor-α), IL-1β, IL-6, MIP-1α (macrophage inflammatory protein-1α) RAGE (receptor for advanced glycation end products), fractalkine, and the IBA-1 microglial marker in most regions tested, with the midbrain showing the greatest DE response. Intratracheal administration of DEP increased microglial IBA-1 staining in the substantia nigra and elevated both serum and whole-brain TNFα at 6 hr posttreatment. Although DEP alone failed to cause the production of cytokines and chemokines, DEP (5 μg/mL) pretreatment followed by lipopolysaccharide (2.5 ng/mL) in vitro synergistically amplified nitric oxide production, TNFα release, and DA neurotoxicity. Pretreatment with fractalkine (50 pg/mL) in vitro ameliorated DEP (50 μg/mL)-induced microglial hydrogen peroxide production and DA neurotoxicity.
Conclusions: Together, these findings reveal complex, interacting mechanisms responsible for how air pollution may cause neuroinflammation and DA neurotoxicity.
TL;DR: A two-hit animal model involving both a genetic lesion and an environmental trigger reproduced key features of PD and demonstrated synergistic effects of genetic predisposition and environmental exposures in the development of PD.
Abstract: BackgroundMechanisms whereby gene–environment interactions mediate chronic, progressive neurodegenerative processes in Parkinson’s disease (PD)—the second most common neurodegenerative disease—rema...
TL;DR: The increased hazard for developmental neurotoxicity by hydroxylated (OH-)PBDEs compared with their parent congeners via direct neurotoxicity and thyroid disruption clearly warrants further investigation into a) the role of oxidative metabolism in producing active metabolites of PBDEs and their impact on brain development; b) concentrations of parent and OH-PBDES in the brain; and c) interactions between different environmental contaminants during exposure to mixtures, which may increase neurotoxicity.
Abstract: Background/objective: Polybrominated diphenyl ethers (PBDEs) and their hydroxylated (OH-) or methoxylated forms have been detected in humans. Because this raises concern about adverse effects on the developing brain, we reviewed the scientific literature on these mechanisms.
Data synthesis: Many rodent studies reported behavioral changes after developmental, neonatal, or adult exposure to PBDEs, and other studies documented subtle structural and functional alterations in brains of PBDE-exposed animals. Functional effects have been observed on synaptic plasticity and the glutamate–nitric oxide–cyclic guanosine monophosphate pathway. In the brain, changes have been observed in the expression of genes and proteins involved in synapse and axon formation, neuronal morphology, cell migration, synaptic plasticity, ion channels, and vesicular neurotransmitter release. Cellular and molecular mechanisms include effects on neuronal viability
(via apoptosis and oxidative stress), neuronal differentiation and migration, neurotransmitter release/uptake, neurotransmitter receptors and ion channels, calcium (Ca2+) homeostasis, and intracellular signaling pathways.
Discussion: Bioactivation of PBDEs by hydroxylation has been observed for several endocrine end points. This has also been observed for mechanisms related to neurodevelopment, including binding to thyroid hormone receptors and transport proteins, disruption of Ca2+ homeostasis, and modulation of GABA and nicotinic acetylcholine receptor function.
Conclusions: The increased hazard for developmental neurotoxicity by hydroxylated (OH-)PBDEs compared with their parent congeners via direct neurotoxicity and thyroid disruption clearly warrants further investigation into a) the role of oxidative metabolism in producing active metabolites of PBDEs and their impact on brain development; b) concentrations of parent and OH-PBDEs in the brain; and c) interactions between different environmental contaminants during exposure to mixtures, which may increase neurotoxicity.
TL;DR: The results support previous reports of associations between phthalates—and possibly BPA—and altered thyroid hormones and the potential clinical and public health implications of these associations.
Abstract: Background: Limited animal, in vitro, and human studies have reported that exposure to phthalates or bisphenol A (BPA) may affect thyroid signaling.Objective: We explored the cross-sectional relati...
TL;DR: This is the first study to demonstrate both respiratory and cardiac effects after brief exposure to peat wildfire smoke in rural counties with sparse air-quality monitoring.
Abstract: Background: In June 2008, burning peat deposits produced haze and air pollution far in excess of National Ambient Air Quality Standards, encroaching on rural communities of eastern North Carolina. Although the association of mortality and morbidity with exposure to urban air pollution is well established, the health effects associated with exposure to wildfire emissions are less well understood.
Objective: We investigated the effects of exposure on cardiorespiratory outcomes in the population affected by the fire.
Methods: We performed a population-based study using emergency department (ED) visits reported through the syndromic surveillance program NC DETECT (North Carolina Disease Event Tracking and Epidemiologic Collection Tool). We used aerosol optical depth measured by a satellite to determine a high-exposure window and distinguish counties most impacted by the dense smoke plume from surrounding referent counties. Poisson log-linear regression with a 5-day distributed lag was used to estimate changes in the cumulative relative risk (RR).
Results: In the exposed counties, significant increases in cumulative RR for asthma [1.65 (95% confidence interval, 1.25–2.1)], chronic obstructive pulmonary disease [1.73 (1.06–2.83)], and pneumonia and acute bronchitis [1.59 (1.07–2.34)] were observed. ED visits associated with cardiopulmonary symptoms [1.23 (1.06–1.43)] and heart failure [1.37 (1.01–1.85)] were also significantly increased.
Conclusions: Satellite data and syndromic surveillance were combined to assess the health impacts of wildfire smoke in rural counties with sparse air-quality monitoring. This is the first study to demonstrate both respiratory and cardiac effects after brief exposure to peat wildfire smoke.
TL;DR: The estimated salt intake from drinking water in this population of rural coastal Bangladesh exceeded recommended limits and is likely to be exacerbated by climate change–induced sea-level rise.
Abstract: Background: Drinking water from natural sources in coastal Bangladesh has become contaminated by varying degrees of salinity due to saltwater intrusion from rising sea levels, cyclone and storm surges and upstream withdrawal of freshwater Objective: Our objective was to estimate salt intake from drinking water sources and examine environmental factors that may explain a seasonal excess of hypertension in pregnancy Methods: Water salinity data (1998-2000) for Dacope, in rural coastal Bangladesh, were obtained from the Centre for Environment and Geographic Information System Information on drinking water sources, 24-hour urine samples and blood pressure were obtained from 343 pregnant Dacope women during the dry season (October 2009 - March 2010) The hospital-based prevalence of hypertension in pregnancy was determined for 969 pregnant women (July 2008 - March 2010) Results: Average estimated sodium intakes from drinking water ranged from 5 to 16 g/day in the dry season, compared to 06 - 12 g/day in the rainy season Average daily sodium excretion in urine was 34 g/day (range 04 - 77 g/d) Women who drank shallow tubewell water were more likely to have urine sodium > 100 mmol/d than women who drank rainwater (OR=205, 95% CI: 111 - 380) The annual hospital prevalence of hypertension in pregnancy was higher in the dry season (122%, 95% CI: 95 - 148) than the rainy season (51%, 95% CI: 291 - 726) Conclusions: The estimated salt intake from drinking water in this population exceeded recommended limits The problem of saline intrusion into drinking water has multiple causes and is likely to be exacerbated by climate change induced sea-level rise
TL;DR: The results strongly suggest that polyhalogenated bisphenols could function as obesogens by acting as agonists to disrupt physiological functions regulated by human or animal PPARγ.
Abstract: Background: The occurrence of halogenated analogs of the xenoestrogen bisphenol A (BPA) has been recently demonstrated both in environmental and human samples. These analogs include brominated [e.g., tetrabromobisphenol A (TBBPA)] and chlorinated [e.g., tetrachlorobisphenol A (TCBPA)] bisphenols, which are both flame retardants. Because of their structural homology with BPA, such chemicals are candidate endocrine disruptors. However, their possible target(s) within the nuclear hormone receptor superfamily has remained unknown.
Objectives: We investigated whether BPA and its halogenated analogs could be ligands of estrogen receptors (ERs) and peroxisome proliferator–activated receptors (PPARs) and act as endocrine-disrupting chemicals.
Methods: We studied the activity of compounds using reporter cell lines expressing ERs and PPARs. We measured the binding affinities to PPARγ by competitive binding assays with [3H]-rosiglitazone and investigated the impact of TBBPA and TCBPA on adipocyte differentiation using NIH3T3-L1 cells. Finally, we determined the binding mode of halogenated BPAs to PPARγ by X-ray crystallography.
Results: We observed that TBBPA and TCBPA are human, zebrafish, and Xenopus PPARγ ligands and determined the mechanism by which these chemicals bind to and activate PPARγ. We also found evidence that activation of ERα, ERβ, and PPARγ depends on the degree of halogenation in BPA analogs. We observed that the bulkier brominated BPA analogs, the greater their capability to activate PPARγ and the weaker their estrogenic potential.
Conclusions: Our results strongly suggest that polyhalogenated bisphenols could function as obesogens by acting as agonists to disrupt physiological functions regulated by human or animal PPARγ.
TL;DR: Of interest, when the population investigated is sufficiently large and samples are randomly collected relative to meal ingestion times and bladder emptying times, the single spot–sampling approach may adequately reflect the average exposure of the population to BPA.
Abstract: Background: Human exposure to bisphenol A (BPA) is widespread. After exposure, BPA is rapidly metabolized and eliminated in urine. Therefore, there is considerable within-person and between-person ...
TL;DR: Certain prenatal phthalate exposures may decrease child mental and motor development and increase internalizing behaviors.
Abstract: Background: Research suggests that prenatal phthalate exposures affect child executive function and behavior.
Objective: We evaluated associations between phthalate metabolite concentrations in maternal prenatal urine and mental, motor, and behavioral development in children at 3 years of age.
Methods: Mono-n-butyl phthalate (MnBP), monobenzyl phthalate (MBzP), monoisobutyl phthalate (MiBP), and four di-2-ethylhexyl phthalate metabolites were measured in a spot urine sample collected from 319 women during the third trimester. When children were 3 years of age, the Mental Development Index (MDI) and Psychomotor Development Index (PDI) were measured using the Bayley Scales of Infant Development II, and behavior problems were assessed by maternal report on the Child Behavior Checklist.
Results: Child PDI scores decreased with increasing loge MnBP [estimated adjusted β-coefficient = –2.81; 95% confidence interval (CI): –4.63, –1.0] and loge MiBP (β = –2.28; 95% CI: –3.90, –0.67); odds of motor delay increased significantly [per loge MnBP: estimated adjusted odds ratio (OR) = 1.64; 95% CI: 1.10, 2.44; per loge MiBP: adjusted OR =1.82; 95% CI: 1.24, 2.66]. In girls, MDI scores decreased with increasing loge MnBP (β = –2.67; 95% CI: –4.70, –0.65); the child sex difference in odds of mental delay was significant (p = 0.037). The ORs for clinically withdrawn behavior were 2.23 (95% CI: 1.27, 3.92) and 1.57 (95% CI: 1.07, 2.31) per loge unit increase in MnBP and MBzP, respectively; for clinically internalizing behaviors, the OR was 1.43 (95% CI: 1.01, 1.90) per loge unit increase in MBzP. Significant child sex differences were seen in associations between MnBP and MBzP and behaviors in internalizing domains (p < 0.05).
Conclusion: Certain prenatal phthalate exposures may decrease child mental and motor development and increase internalizing behaviors.
TL;DR: An association between arsenic and the prevalence of hypertension is identified and a dose–response assessment including six studies with available data showed an increasing trend in the odds of hypertension with increasing arsenic exposure.
Abstract: Background: Environmental exposure to arsenic has been linked to hypertension in persons living in arsenic-endemic areas.
Objective: We summarized published epidemiologic studies concerning arsenic exposure and hypertension or blood pressure (BP) measurements to evaluate the potential relationship.
Data sources and extraction: We searched PubMed, Embase, and TOXLINE and applied predetermined exclusion criteria. We identified 11 cross-sectional studies from which we abstracted or derived measures of association and calculated pooled odds ratios (ORs) using inverse-variance weighted random-effects models.
Data synthesis: The pooled OR for hypertension comparing the highest and lowest arsenic exposure categories was 1.27 [95% confidence interval (CI): 1.09, 1.47; p-value for heterogeneity = 0.001; I2 = 70.2%]. In populations with moderate to high arsenic concentrations in drinking water, the pooled OR was 1.15 (95% CI: 0.96, 1.37; p-value for heterogeneity = 0.002; I2 = 76.6%) and 2.57 (95% CI: 1.56, 4.24; p-value for heterogeneity = 0.13; I2 = 46.6%) before and after excluding an influential study, respectively. The corresponding pooled OR in populations with low arsenic concentrations in drinking water was 1.56 (95% CI: 1.21, 2.01; p-value for heterogeneity = 0.27; I2 = 24.6%). A dose–response assessment including six studies with available data showed an increasing trend in the odds of hypertension with increasing arsenic exposure. Few studies have evaluated changes in systolic and diastolic BP (SBP and DBP, respectively) measurements by arsenic exposure levels, and those studies reported inconclusive findings.
Conclusion: In this systematic review we identified an association between arsenic and the prevalence of hypertension. Interpreting a causal effect of environmental arsenic on hypertension is limited by the small number of studies, the presence of influential studies, and the absence of prospective evidence. Additional evidence is needed to evaluate the dose–response relationship between environmental arsenic exposure and hypertension.
TL;DR: It is suggested that significant health and economic benefits are possible if bicycling replaces short car trips and the combined benefits of improved air quality and physical fitness would exceed $8 billion/year.
Abstract: Background: Automobile exhaust contains precursors to ozone and fine particulate matter (PM ≤ 2.5 µm in aerodynamic diameter; PM2.5), posing health risks. Dependency on car commuting also reduces physical fitness opportunities.
Objective: In this study we sought to quantify benefits from reducing automobile usage for short urban and suburban trips.
Methods: We simulated census-tract level changes in hourly pollutant concentrations from the elimination of automobile round trips ≤ 8 km in 11 metropolitan areas in the upper midwestern United States using the Community Multiscale Air Quality (CMAQ) model. Next, we estimated annual changes in health outcomes and monetary costs expected from pollution changes using the U.S. Environmental Protection Agency Benefits Mapping Analysis Program (BenMAP). In addition, we used the World Health Organization Health Economic Assessment Tool (HEAT) to calculate benefits of increased physical activity if 50% of short trips were made by bicycle.
Results: We estimate that, by eliminating these short automobile trips, annual average urban PM2.5 would decline by 0.1 µg/m3 and that summer ozone (O3) would increase slightly in cities but decline regionally, resulting in net health bene-fits of $4.94 billion/year [95% confidence interval (CI): $0.2 billion, $13.5 billion), with 25% of PM2.5 and most O3 bene-fits to populations outside metropolitan areas. Across the study region of approximately 31.3 million people and 37,000 total square miles, mortality would decline by approximately 1,295 deaths/year (95% CI: 912, 1,636) because of improved air quality and increased exercise. Making 50% of short trips by bicycle would yield savings of approximately $3.8 billion/year from avoided mortality and reduced health care costs (95% CI: $2.7 billion, $5.0 billion]. We estimate that the combined benefits of improved air quality and physical fitness would exceed $8 billion/year.
Conclusion: Our findings suggest that significant health and economic benefits are possible if bicycling replaces short car trips. Less dependence on automobiles in urban areas would also improve health in downwind rural settings.
TL;DR: PM2.5 exposure from biomass combustion may be a risk factor for elevated BP and hence for cardiovascular events and should be corroborated in longitudinal studies.
Abstract: Background: Almost half of the world’s population uses coal and biomass fuels for domestic energy. Limited evidence suggests that exposure to air pollutants from indoor biomass combustion may be as...