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\"Freshwater Algae provides a comprehensive guide to temperate freshwater algae, with additional information on key species in relation to environmental characteristics and implications for aquatic management.Existing books on freshwater algae fall into two categories: simple identification texts or highly specialised research volumes. There is currently nothing in between that practitioners and students can use on a regular basis. The authors filled this gap with the first edition which provided an accessible, visually appealing volume that is of immediate use to aquatic biologists for algal identification that includes key environmental information on major species.The book is divided into two parts: part I is a general introduction to algae and techniques for sampling, measuring and observation and then looks at the role of algae as bioindicators and the implications for aquatic management, part II provides the identification of major genera and 250 important species. The book is well illustrated in full colour with numerous original illustrations and photographs. This new revised edition will retain the same clear writing style and accessible format of the first edition with new coverage of species from North America, Asia and Australia in addition to expanded coverage of molecular and computational techniques in algal biology\"-- Provided by publisher.

Background: The impact of environmental chemicals on children's neurodevelopment is sometimes dismissed as unimportant because the magnitude of the impairments are considered to be clinically insignificant. Such a judgment reflects a failure to distinguish between individual and population risk. The population impact of a risk factor depends on both its effect size and its distribution (or incidence/prevalence). Objective: The objective was to develop a strategy for taking into account the distribution (or incidence/prevalence) of a risk factor, as well as its effect size, in order to estimate its population impact on neurodevelopment of children. Methods: The total numbers of Full-Scale IQ points lost among U. S. children 0-5 years of age were estimated for chemicals (methylmercury, organophosphate pesticides, lead) and a variety of medical conditions and events (e.g., preterm birth, traumatic brain injury, brain tumors, congenital heart disease). Discussion: Although the data required for the analysis were available for only three environmental chemicals (methylmercury, organophosphate pesticides, lead), the results suggest that their contributions to neurodevelopmental morbidity are substantial, exceeding those of many nonchemical risk factors. Conclusion: A method for comparing the relative contributions of different risk factors provides a rational basis for establishing priorities for reducing neurodevelopmental morbidity in children.

Exposure to chemical mixtures is recognized as the real-life scenario in all populations, needing new statistical methods that can assess their complex effects. We aimed to assess the joint effect of in utero exposure to arsenic, manganese, and lead on children's neurodevelopment. We employed a novel statistical approach, Bayesian kernel machine regression (BKMR), to study the joint effect of coexposure to arsenic, manganese, and lead on neurodevelopment using an adapted Bayley Scale of Infant and Toddler Development™. Third Edition, in 825 mother-child pairs recruited into a prospective birth cohort from two clinics in the Pabna and Sirajdikhan districts of Bangladesh. Metals were measured in cord blood using inductively coupled plasma-mass spectrometry. Analyses were stratified by clinic due to differences in exposure profiles. In the Pabna district, which displayed high manganese levels [interquartile range (IQR): 4.8, 18 μg/dl], we found a statistically significant negative effect of the mixture of arsenic, lead, and manganese on cognitive score when cord blood metals concentrations were all above the 60th percentile (As≥0.7 μg/dl, Mn≥6.6 μg/dl, Pb≥4.2 μg/dl) compared to the median (As=0.5 μg/dl, Mn=5.8 μg/dl, Pb=3.1 μg/dl). Evidence of a nonlinear effect of manganese was found. A change in log manganese from the 25th to the 75th percentile when arsenic and manganese were at the median was associated with a decrease in cognitive score of −0.3 (−0.5, −0.1) standard deviations. Our study suggests that arsenic might be a potentiator of manganese toxicity. Employing a novel statistical method for the study of the health effects of chemical mixtures, we found evidence of neurotoxicity of the mixture, as well as potential synergism between arsenic and manganese. https://doi.org/10.1289/EHP614.

Manganese neurotoxicity is well documented in individuals occupationally exposed to airborne particulates, but few data are available on risks from drinking-water exposure. We examined associations of exposure from concentrations of manganese in water and hair with memory, attention, motor function, and parent- and teacher-reported hyperactive behaviors. We recruited 375 children and measured manganese in home tap water (MnW) and hair (MnH). We estimated manganese intake from water ingestion. Using structural equation modeling, we estimated associations between neurobehavioral functions and MnH, MnW, and manganese intake from water. We evaluated exposure-response relationships using generalized additive models. After adjusting for potential confounders, a 1-SD increase in log10 MnH was associated with a significant difference of -24% (95% CI: -36, -12%) SD in memory and -25% (95% CI: -41, -9%) SD in attention. The relations between log10 MnH and poorer memory and attention were linear. A 1-SD increase in log10 MnW was associated with a significant difference of -14% (95% CI: -24, -4%) SD in memory, and this relation was nonlinear, with a steeper decline in performance at MnW > 100 μg/L. A 1-SD increase in log10 manganese intake from water was associated with a significant difference of -11% (95% CI: -21, -0.4%) SD in motor function. The relation between log10 manganese intake and poorer motor function was linear. There was no significant association between manganese exposure and hyperactivity. Exposure to manganese in water was associated with poorer neurobehavioral performances in children, even at low levels commonly encountered in North America.

Background: Manganese is an essential nutrient, but in excess it can be a potent neurotoxicant. Despite the common occurrence of manganese in groundwater, the risks associated with this source of exposure are largely unknown. Objectives: Our first aim was to assess the relations between exposure to manganese from drinking water and children's intelligence quotient (IQ). Second, we examined the relations between manganese exposures from water consumption and from the diet with children's hair manganese concentration. Methods: This cross-sectional study included 362 children 6—13 years of age living in communities supplied by groundwater. Manganese concentration was measured in home tap water (MnW) and children's hair (MnH). We estimated manganese intake from water ingestion and the diet using a food frequency questionnaire and assessed IQ with the Wechsler Abbreviated Scale of Intelligence. Results: The median MnW in children's home tap water was 34 µg/L (range, 1-2,700 µg/L). MnH increased with manganese intake from water consumption, but not with dietary manganese intake. Higher MnW and MnH were significantly associated with lower IQ scores. A 10-fold increase in MnW was associated with a decrease of 2.4 IQ points (95% confidence interval: — 3.9 to -0.9; p < 0.01), adjusting for maternal intelligence, family income, and other potential confounders. There was a 6.2-point difference in IQ between children in the lowest and highest MnW quintiles. MnW was more strongly associated with Performance IQ than Verbal IQ. Conclusions: The findings of this cross-sectional study suggest that exposure to manganese at levels common in groundwater is associated with intellectual impairment in children.

The recent episode in Flint, Michigan, has brought the issue of lead in water into the public eye. But the dangers of lead exposure have been recognized for millennia, and we have the knowledge required to redress this social crime — if only we had the political will. The dangers of lead exposure have been recognized for millennia. In the first century a.d., Dioscorides observed in his De Materia Medica that “lead makes the mind give way.” The first industrial hygiene act passed in the colonies, in 1723, prohibited the use of lead in the apparatus used to distill rum, because “the strong liquors and spirits that are distilld through leaden heads or pipes are judged on good grounds to be unwholsom and hurtful.” More recently, large amounts of lead were used to boost the octane rating of gasoline and improve the performance of paint. One would be . . .

Background A growing body of epidemiologic and toxicologic literature indicates that fine airborne particulate matter (PM 2.5 ) pollution is neurotoxic and threatens children’s neurobehavioral development, resulting in reduced cognitive function. Understanding the magnitude of this effect is critical for establishing public health policies that will protect children’s health, preserve human capital, and support societal progress. Objective To quantify the association between ambient PM 2.5 air pollution and loss of cognitive function in children, as measured by Intelligence Quotient (IQ) scores, through a systematic literature review and meta-analysis. Methods Following PRISMA guidelines, we conducted a systematic literature search across seven databases: Agricultural and Environmental Science, BIOSIS Citation Index, Embase, GreenFILE, PubMed, Scopus, and Web of Science to identify original scientific studies that investigated the impact of PM 2.5 exposure during pre-and postnatal periods on IQ loss during childhood. Using data from studies included for final review, we conducted a meta-analysis, using a random effects model to compute a beta coefficient that quantifies the overall effect of PM 2.5 exposure on Full-Scale IQ (FSIQ), Performance IQ (PIQ), and Verbal IQ (VIQ). Findings Of the 1,107 unique publications identified, six studies met the inclusion criteria for final review, representing 4,860 children across three continents (North America, Europe, and Asia). The mean PM 2.5 concentration across all studies was 30.4 ± 24.4 µg/m 3 . Exposure timing ranged from the prenatal period to mid-childhood. Children were an average of 8.9 years old at the time of cognitive testing. We found that each 1 µg/m 3 increase in PM 2.5 concentration is associated with a -0.27 point change in FSIQ ( p  < 0.001), 0.39 point change in PIQ ( p  = 0.003), and -0.24 point change in VIQ ( p  = 0.021). Conclusion Through a systematic review and meta-analysis, we identified a statistically significant relationship between increased exposure to PM 2.5 air pollution and reduced cognitive function in children, with the most pronounced impact on PIQ. This analysis will enable estimation of the burden of adverse neurobehavioral development attributable to PM 2.5 in pediatric populations and will inform local and global strategies for exposure prevention.

The purpose of this commentary is to consider whether the methods of the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) can provide accurate estimates of the impact of developmental neurotoxicant exposures on population health. The discussion focuses on two concerns. First, GBD implicitly largely endorses a “high risk” or “disease” approach to estimating health loss rather than a “population-based” approach. Exposure to many developmental neurotoxicants is highly prevalent but, for most individuals, it does not affect functional health to such an extent that diagnostic criteria for a disease are met. Nevertheless, the impacts are real and can be substantial when viewed in terms of the aggregate impact on a population. Second, in GBD the disability weights used for the most common sequelae of developmental neurotoxicant exposures, based on judgments provided by general population respondents, are not commensurate with the import that these sequelae have for an individual’s lifelong well-being, including their ability to fulfill educational, occupational, and social potential. It would be unfortunate if priorities were set or policy decisions made based on how developmental neurotoxicants compare to other risk factors using the current GBD methods.

Background: In animal studies, perfluorinated compounds affect fetal growth, development, viability, and postnatal growth. The limited epidemiologic findings on child neurobehavioral development are mixed. Methods: We recruited and evaluated 320 children who participated in the C8 Health Project, a 2005—2006 survey in a Mid-Ohio Valley community highly exposed to perfluorooctanoate (PFOA) through contaminated drinking water. We examined associations among estimated in utero PFOA exposure, measured childhood PFOA serum concentration, and subsequent performance on neuropsychological tests 3—4 years later at ages 6—12 years. We assessed Intelligence Quotient (IQ) reading and math skills, language, memory and learning, visual-spatial processing, and attention. All multivariable linear regression models were adjusted for age, sex, home environment, test examiner, and maternal IQ. Models with measured childhood PFOA were additionally adjusted for child body mass index. Results: Children in the highest as compared with lowest quartile of estimated in utero PFOA had increases in Full Scale IQ (β 4.6, 95% confidence interval [CI] = 0.7—8.5) and decreases in characteristics of attention deficit/hyperactivity disorder as measured by the Clinical Confidence Index of Connors' Continuous Performance Test—II (β -8.5, 95% CI = -16.1 to -0.8). There were negligible associations between PFOA and reading or math skills or neuropsychological functioning. Conclusion: These results do not suggest an adverse association between the levels of PFOA exposure experienced by children in this cohort and their performance on neuropsychological tests.