From minerals to rocks: Toward modeling lithologies with remote sensing

High spectral resolution imaging spectroscopy will play an important role in future planetary missions. Sophisticated approaches will be needed to unravel subtle, super-imposed spectral features typically of natural systems, and to maximize the science return of these instruments. Carefully controlled laboratory investigations using homogeneous mineral separates have demonstrated that variations due to solid solution, changes in modal abundances, and the effects of particle size are well understood from a physical basis. In many cases, these variations can be modeled quantitatively using photometric models, mixing approaches, and deconvolution procedures. However, relative to the spectra of individual mineral components, reflectance spectra of rocks and natural surfaces exhibit a reduced spectral contrast. In addition, soils or regolith, which are likely to dominate any natural planetary surface, exhibit spectral properties that have some similarities to the parent materials, but due to weathering and alteration, differences remain that cannot yet be fully recreated in the laboratory or through mixture modeling. A significant challenge is therefore to integrate modeling approaches to derive both lithologic determinations and include the effects of alteration. We are currently conducting laboratory investigations in lithologic modeling to expand upon the basic results of previous analyses with our initial goal to more closely match physical state of natural systems. The effects of alteration are to be considered separately

Induction of Asthma and the Environment: What We Know and Need to Know

The prevalence of asthma has increased dramatically over the last 25 years in the United States and in other nations as a result of ill-defined changes in living conditions in modern society. On 18 and 19 October 2004 the U.S. Environmental Protection Agency and the National Institute of Environmental Health Sciences sponsored the workshop “Environmental Influences on the Induction and Incidence of Asthma” to review current scientific evidence with respect to factors that may contribute to the induction of asthma. Participants addressed two broad questions: a) What does the science suggest that regulatory and public health agencies could do now to reduce the incidence of asthma? and b) What research is needed to improve our understanding of the factors that contribute to the induction of asthma and our ability to manage this problem? In this article (one of four articles resulting from the workshop), we briefly characterize asthma and its public health and economic impacts, and intervention strategies that have been successfully used to prevent induction of asthma in the workplace. We conclude with the findings of seven working groups that focus on ambient air, indoor pollutants (biologics), occupational exposures, early life stages, older adults, intrinsic susceptibility, and lifestyle. These groups found strong scientific support for public health efforts to limit in utero and postnatal exposure to cigarette smoke. However, with respect to other potential types of interventions, participants noted many scientific questions, which are summarized in this article. Research to address these questions could have a significant public health and economic impact that would be well worth the investment

Meeting Report: Consensus Statement—Parkinson’s Disease and the Environment: Collaborative on Health and the Environment and Parkinson’s Action Network (CHE PAN) Conference 26–28 June 2007

BackgroundParkinson's disease (PD) is the second most common neurodegenerative disorder. People with PD, their families, scientists, health care providers, and the general public are increasingly interested in identifying environmental contributors to PD risk.MethodsIn June 2007, a multidisciplinary group of experts gathered in Sunnyvale, California, USA, to assess what is known about the contribution of environmental factors to PD.ResultsWe describe the conclusions around which they came to consensus with respect to environmental contributors to PD risk. We conclude with a brief summary of research needs.ConclusionsPD is a complex disorder, and multiple different pathogenic pathways and mechanisms can ultimately lead to PD. Within the individual there are many determinants of PD risk, and within populations, the causes of PD are heterogeneous. Although rare recognized genetic mutations are sufficient to cause PD, these account for < 10% of PD in the U.S. population, and incomplete penetrance suggests that environmental factors may be involved. Indeed, interplay among environmental factors and genetic makeup likely influences the risk of developing PD. There is a need for further understanding of how risk factors interact, and studying PD is likely to increase understanding of other neurodegenerative disorders

Prevalence of allergic sensitization in the U.S.: Results from the National Health and Nutrition Examination Survey (NHANES) 2005–2006

Allergic sensitization is an important risk factor for the development of atopic disease. The National Health and Nutrition Examination Survey (NHANES) 2005–2006 provides the most comprehensive information on IgE-mediated sensitization in the general US population

A Quantitative Approach for Estimating Exposure to Pesticides in the Agricultural Health Study

We developed a quantitative method to estimate long-term chemical-specific pesticide exposures in a large prospective cohort study of more than 58000 pesticide applicators in North Carolina and Iowa. An enrollment questionnaire was administered to applicators to collect basic time- and intensity-related information on pesticide exposure such as mixing condition, duration and frequency of application, application methods and personal protective equipment used. In addition, a detailed take-home questionnaire was administered to collect further intensity- related exposure information such as maintenance or repair of mixing and application equipment, work practices and personal hygiene. More than 40% of the enrolled applicators responded to this detailed take-home questionnaire. Two algorithms were developed to identify applicators’ exposure scenarios using information from the enrollment and take-home questionnaires separately in the calculation of subject-specific intensity of exposure score to individual pesticides. The ‘general algorithm’ used four basic variables (i.e. mixing status, application method, equipment repair status and personal protective equipment use) from the enrollment questionnaire and measurement data from the published pesticide exposure literature to calculate estimated intensity of exposure to individual pesticides for each applicator. The ‘detailed’ algorithm was based on variables in the general algorithm plus additional exposure information from the take-home questionnaire, including types of mixing system used (i.e. enclosed or open), having a tractor with enclosed cab and/or charcoal filter, frequency of washing equipment after application, frequency of replacing old gloves, personal hygiene and changing clothes after a spill. Weighting factors applied in both algorithms were estimated using measurement data from the published pesticide exposure literature and professional judgment. For each study subject, chemical-specific lifetime cumulative pesticide exposure levels were derived by combining intensity of pesticide exposure as calculated by the two algorithms independently and duration/frequency of pesticide use from the questionnaire. Distributions of duration, intensity and cumulative exposure levels of 2,4-D and chlorpyrifos are presented by state, gender, age group and applicator type (i.e. farmer or commercial applicator) for the entire enrollment cohort and for the sub-cohort of applicators who responded to the take-home questionnaire. The distribution patterns of all basic exposure indices (i.e. intensity, duration and cumulative exposure to 2,4-D and chlorpyrifos) by state, gender, age and applicator type were almost identical in two study populations, indicating that the take-home questionnaire sub-cohort of applicators is representative of the entire cohort in terms of exposure

Pyrimethanil and chlorpyrifos air concentrations and pregnant women's urinary metabolites in the Infants’ Environmental Health Study (ISA), Costa Rica

Background: Only few studies have compared environmental pesticide air concentrations with specific urinary metabolites to evaluate pathways of exposure. Therefore, we compared pyrimethanil and chlorpyrifos concentrations in air with urinary 4-hydroxypyrimethanil (OHP, metabolite of pyrimethanil) and 3,5,6-trichloro-2-pyridinol (TCPy, metabolite of chlorpyrifos) among pregnant women from the Infant's Environmental Health Study (ISA) in Matina County, Costa Rica. Methods: During pregnancy, we obtained repeat urinary samples from 448 women enrolled in the ISA study. We extrapolated pyrimethanil and chlorpyrifos concentrations measured with passive air samplers (PAS) (n = 48, from 12 schools), across space and time using a Bayesian spatiotemporal model. We subsequently compared these concentrations with urinary OHP and TCPy in 915 samples from 448 women, using separate mixed models and considering several covariables. Results: A 10% increase in air pyrimethanil (ng/m3) was associated with a 5.7% (95% confidence interval (CI 4.6, 6.8) increase in OHP (μg/L). Women living further from banana plantations had lower OHP: −0.7% (95% CI −1.2, −0.3) for each 10% increase in distance (meters) as well as women who ate rice and beans ≥15 times a week −23% (95% CI −38, −4). In addition, each 1 ng/m3 increase in chlorpyrifos in air was associated with a 1.5% (95% CI 0.2, 2.8) increase in TCPy (μg/L), and women working in agriculture tended to have increased TCPy (21%, 95% CI −2, 49). Conclusion: The Bayesian spatiotemporal models were useful to estimate pyrimethanil and chlorpyrifos air concentrations across space and time. Our results suggest inhalation of pyrimethanil and chlorpyrifos is a pathway of environmental exposure. PAS seems a useful technique to monitor environmental current-use pesticide exposures. For future studies, we recommend increasing the number of locations of environmental air measurements, obtaining all air and urine measurements during the same month, and, ideally, including dermal exposure estimates as well

Exposure to common-use pesticides, manganese, lead, and thyroid function among pregnant women from the Infants Environmental Health (ISA) study, Costa Rica.

BACKGROUND: Pesticides and metals may disrupt thyroid function, which is key to fetal brain development. OBJECTIVES: To evaluate if current-use pesticide exposures, lead and excess manganese alter free thyroxine (FT4), free triiodothyronine (FT3), and thyroid stimulating hormone (TSH) concentrations in pregnant women from the Infants Environmental Health Study (ISA). METHODS: At enrollment, we determined womens (n = 400) specific-gravity corrected urinary pesticide (μg/L) metabolite concentrations of mancozeb (ethylene thiourea (ETU)), pyrimethanil, thiabendazole, chlorpyrifos, synthetic pyrethroids, and 2,4-D. We also measured manganese hair (MnH) (μg/g) and blood (MnB) (μg/L), and blood lead (PbB) (μg/L) concentrations. To detect an immediate and late effect on thyroid homeostasis, we determined TSH, FT4 and FT3 in serum obtained at the same visit (n = 400), and about ten weeks afterwards (n = 245). We assessed associations between exposures and outcomes with linear regression and general additive models, Bayesian multivariate linear regression, and Bayesian kernel machine regression. RESULTS: About 80%, 94%, and 100% of the women had TSH, FT4, and FT3 within clinical reference ranges, respectively. Women with higher urinary ETU, and pyrimethanil-metabolites, had lower FT4: β = -0.79 (95%CI = -1.51, -0.08) and β = -0.29 (95%CI = -0.62, -0.03), respectively, for each tenfold increase in exposure. MnB was positively associated with FT4 (β = 0.04 (95%CI = 0.00, 0.07 per 1 μg/L increase), and women with high urinary pyrethroid-metabolite concentrations had decreased TSH (non-linear effects). For the late-effect analysis, metabolites of pyrethroids and chlorpyrifos, as well as MnH, and PbB were associated decreased TSH, or increased FT4 and/or FT3. DISCUSSION: Mancozeb (ETU) and pyrimethanil may inhibit FT4 secretion (hypothyroidism-like effect), while chlorpyrifos, pyrethroids, MnB, MnH, PbB and Mn showed hyperthyroidism-like effects. Some effects on thyroid homeostasis seemed to be immediate (mancozeb (ETU), pyrimethanil, MnB), others delayed (chlorpyrifos, MnH, PbB), or both (pyrethroids), possibly reflecting different mechanisms of action

Exposure to common-use pesticides, manganese, lead, and thyroidfunction among pregnant women from the Infants' EnvironmentalHealth (ISA) study, Costa Rica

Programa Infantes y Salud AmbientalPrograma ISAISAInfants' Environmental Health StudyInfants' Environmental Health ProgramISA birth cohortBackground:Pesticides and metals may disrupt thyroid function, which is key to fetal brain development.Objectives:To evaluate if current-use pesticide exposures, lead and excess manganese alter free thyroxine (FT4),freetriiodothyronine(FT3), and thyroidstimulatinghormone (TSH) concentrationsinpregnant women fromtheInfants' Environmental Health Study (ISA).Methods:At enrollment, we determined women's (n=400)specific-gravity corrected urinary pesticide (μg/L)metabolite concentrations of mancozeb (ethylene thiourea (ETU)), pyrimethanil, thiabendazole, chlorpyrifos,synthetic pyrethroids, and 2,4-D. We also measured manganese hair (MnH) (μg/g) and blood (MnB) (μg/L),and blood lead (PbB) (μg/L) concentrations. To detect an immediate and late effect on thyroid homeostasis, wedetermined TSH, FT4 and FT3 in serum obtained at the same visit (n= 400), and about ten weeks afterwards (n= 245). We assessed associations between exposures and outcomes with linear regression and general addi-tive models, Bayesian multivariate linear regression, and Bayesian kernel machine regression.Results:About 80%, 94%, and 100% of the women had TSH, FT4, and FT3 within clinical reference ranges, respec-tively. Women with higher urinary ETU, and pyrimethanil-metabolites, had lower FT4:β=−0.79 (95%CI =−1.51,−0.08) andβ=−0.29 (95%CI =−0.62,−0.03), respectively, for each tenfold increase in exposure.MnB was positively associated with FT4 (β= 0.04 (95%CI = 0.00, 0.07 per 1μg/L increase), and women withhigh urinary pyrethroid-metabolite concentrations had decreased TSH (non-linear effects). For the late-effectanalysis, metabolites of pyrethroids and chlorpyrifos, as well as MnH, and PbB were associated decreased TSH,or increased FT4 and/or FT3.Discussion:Mancozeb (ETU) and pyrimethanil may inhibit FT4 secretion (hypothyroidism-like effect), whilechlorpyrifos, pyrethroids, MnB, MnH, PbB and Mn showed hyperthyroidism-like effects. Some effects on thyroidhomeostasis seemed to be immediate (mancozeb (ETU), pyrimethanil, MnB), others delayed (chlorpyrifos, MnH,PbB), or both (pyrethroids), possibly reflecting different mechanisms of action.Antecedentes: los pesticidas y los metales pueden alterar la función tiroidea, que es clave para el desarrollo del cerebro fetal.Objetivos: Evaluar si la exposición a pesticidas de uso actual, el plomo y el exceso de manganeso alteran la tiroxina libre (FT4), la triyodotironina libre (FT3) y la hormona estimulante de la tiroides (TSH) Métodos: En el momento de la inscripción, determinamos las concentraciones urinarias de plaguicidas (μg / L) de plaguicida corregido por gravedad específica (μg / L) de mujeres (n = 400) de mancozeb (etilen tiourea (ETU)), pirimetanil, tiabendazol en mujeres embarazadas. , clorpirifos, piretroides sintéticos y 2,4-D. También medimos las concentraciones de manganeso en cabello (MnH) (μg / g) y sangre (MnB) (μg / L), y de plomo en sangre (PbB) (μg / L). Para detectar un efecto inmediato y tardío sobre la homeostasis tiroidea, determinamos TSH, FT4 y FT3 en el suero obtenido en la misma visita (n = 400) y aproximadamente diez semanas después (n = 245). Evaluamos las asociaciones entre las exposiciones y los resultados con regresión lineal y modelos aditivos generales, regresión lineal multivariante bayesiana y regresión de máquina de kernel bayesiana. Resultados: Aproximadamente el 80%, 94% y 100% de las mujeres tenían TSH, FT4 y FT3 dentro de los rangos de referencia clínica, respectivamente. Las mujeres con mayor ETU urinaria y metabolitos de pirimetanilo tenían menor FT4: β = −0,79 (IC del 95% = −1,51, −0,08) y β = −0,29 (IC del 95% = −0,62, −0,03), respectivamente, para cada El MnB se asoció positivamente con FT4 (β = 0,04 (IC del 95% = 0,00, 0,07 por aumento de 1 μg / L), y las mujeres con concentraciones altas de metabolitos piretroides en orina tenían TSH disminuida (efectos no lineales). análisis de efectos tardíos, metabolitos de piretroides y clorpirifos, así como MnH y PbB se asociaron con disminución de TSH o aumento de FT4 y / o FT3. Discusión: Mancozeb (ETU) y pirimetanilo pueden inhibir la secreción de FT4 (efecto similar al hipotiroidismo), mientras que el clorpirifos , piretroides, MnB, MnH, PbB y Mn mostraron efectos similares al hipertiroidismo. Algunos efectos sobre la homeostasis tiroidea parecían ser inmediatos (mancozeb (ETU), pirimetanil, MnB), otros retardados (clorpirifos, MnH, PbB) o ambos (piretroides) , posiblemente reflejando diferentes mecanismos de acción.Universidad Nacional, Costa RicaLund University, SwedenUniversity of California at Berkeley, United StatesFederal University of Bahia, BrasilUniversity of California, United StatesUniversité du Québec à Montréal, CanadaNorth Carolina State University, United StatesInstituto Regional de Estudios en Sustancias Tóxica