Environews
FOCUS | Missing the Dark: Health Effects of Light Pollution
The invention of electric lighting has given modern society the ability to conduct as much activity during the nighttime hours as during the day. While this convenience increases productivity, it comes at a price: light pollution, which recent studies indicate causes lasting health effects beyond simple annoyance. This article (p. A20) discusses how our use of round-the-clock electric lighting affects our health.
SPHERES OF INFLUENCE | Switch On the Night: Policies for Smarter Lighting
In addition to economic consequences of using excessive electric light at night, experts warn that the resultant light pollution impedes basic biological and ecological functions of nature that darkness supports. Now communities throughout the world are working to curtail the unnecessary and inefficient use of electric light at night. This article (p. A28) takes a look at some of the organized efforts on local, national, and international levels seeking to lessen the impact of light pollution.
Commentary
RESPIRATORY DISEASE | Synergy and Air Pollution
Air pollutants are inhaled as complex mixtures, but the focus of monitoring and research has been on individual pollutants; however, this practice does not take into account pollutant interactions that may be important to health. Mauderly and Samet (p. 1) reviewed selected published literature to determine whether combinations of ozone with other pollutants may have synergistic effects on health outcomes. The authors found that synergism involving O3 has been demonstrated by laboratory studies of humans and animals, although comparisons are limited, and most studies involved exposure concentrations much higher than typical of environmental pollutants.
Reviews
NEUROTOXICOLOGY | Neuropsychologic Analysis of Prenatal PCB Effects
Prenatal exposure to polychlorinated biphenyls (PCBs) has been shown to affect cognitive development of children, but the cognitive functions that are particularly affected have not yet been identified. Boucher et al. (p. 7) reviewed data from nine prospective longitudinal birth cohorts to investigate the cognitive profile associated with prenatal PCB exposure. They found that prenatal exposure to environmental levels of PCBs appears to be related to a relatively specific profile of cognitive impairments.
Also see Science Selections, p. A32
NEUROTOXICOLOGY | DNT: Retrospective Performance Assessment
Makris et al. (p. 17) conducted a review of the history and performance of developmental neurotoxicity (DNT) testing based on the Organisation of Economic Co-operation and Development (OECD) DNT test guideline 426 (TG 426). They found that the DNT study, a specialized type of developmental toxicity study, represents the best available science for assessing the potential for DNT in human health risk assessment, and that data generated with this protocol are relevant and reliable for the assessment of these end points. Reproducibility, reliability, and sensitivity have been demonstrated using a wide variety of test substances, in accordance with OECD guidance on the validation and international acceptance of new or updated test methods for hazard characterization.
Research
NUTRITION | Calcium Supplementation and Blood Lead in Pregnancy
Prenatal lead exposure is associated with deficits in fetal growth and neurodevelopment. Calcium supplementation may attenuate fetal exposure by inhibiting mobilization of maternal bone lead and/or intestinal absorption of ingested lead. Ettinger et al. (p. 26) investigated whether 1,200 mg daily calcium supplementation affected maternal blood lead levels during pregnancy, finding modest reductions in blood lead in women randomly assigned to receive calcium supplements during pregnancy. They concluded that calcium supplementation appears to be a cost-effective means for lowering fetal lead exposure.
Also see Science Selections, p. A32
REPRODUCTIVE HEALTH | Effects of Phthalates on the Human Fetal Testis
Phthalate esters represent a class of environmental endocrine-active chemicals known to disrupt development of the male reproductive tract by decreasing testosterone production in the fetal rat. Using an organ culture system, Lambrot et al. (p. 32) investigated the effects of mono-2-ethylhexyl phthalate (an industrial chemical found in many products) on the development of human fetal testis. Phthalates altered the development of cultured human germ cells; however, in contrast to results observed in rats, phthalates did not affect steroidogenesis.
Also see Science Selections, p. A33
CARDIOVASCULAR DISEASE | Diesel Exhaust and Cardiac Gene Expression
Exposure to diesel exhaust (DE) is linked to vasoconstriction, endothelial dysfunction, and myocardial ischemia in compromised individuals. Gottipolu et al. (p. 38) investigated whether DE inhalation would cause greater inflammation, hematologic alterations, and cardiac molecular impairment in spontaneously hypertensive rats than in healthy Wistar Kyoto rats. They found evidence that DE inhalation produces a hypertensive-like cardiac gene expression pattern associated with mitochondrial oxidative stress in healthy rats.
EXPOSURE SCIENCE | U.S. Blood Mercury Concentrations: Regional and Coastal Estimates
Using data from the National Health and Nutrition Examination Survey (NHANES), Mahaffey et al. (p. 47) investigated blood mercury distributions within U.S. Census regions and within coastal and noncoastal areas among women of childbearing age, their association with patterns of fish consumption, and changes from 1999 through 2004. They found blood Hg to be associated with income, ethnicity, and residence (census region and coastal proximity). Over the 6-year period, blood Hg decreased without a significant decrease in fish consumption. This suggests a change in type of fish eaten rather than a reduction in fish consumption.
NANOTECHNOLOGY | Origin of Particle-Related Oxidative Stress
Stoeger et al. (p. 54) assessed whether the in vivo inflammatory response of mice to combustion-derived nanoparticles (CDNPs) can be predicted in vitro by a cell-free test for oxidative potency (OxPot) of particles and a gene expression analysis targeting inflammation, stress, and detoxification-related genes. They found a correlation between inflammatory response and Brunauer, Emmett, and Teller (BET) surface area for all CDNPs, and derived a simple quantitative model to predict in vivo inflammatory response based on in vitro OxPot and Cyp1a1 induction. This model may serve as an additional step toward introducing a cell-free test for nanotoxicology that is reliable enough to provide a true alternative to animal exposures.
CLIMATE CHANGE | 2006 California Heat-Wave Hospital and ED Visits
Climate models project that heat waves will increase in frequency and severity. Despite many studies of mortality from heat waves, few studies have examined morbidity. Knowlton et al. (p. 61) investigated whether any age or race/ethnicity groups experienced increased hospitalizations and emergency department visits overall or for selected illnesses during the 2006 California heat wave. This heat wave had a substantial effect on morbidity, including regions with relatively modest absolute temperatures. This suggests that population acclimatization and adaptive capacity influenced risk. By better understanding these impacts and population vulnerabilities, local communities can improve heat-wave preparedness to cope with a globally warming future.
NEURODEVELOPMENT | Embryonic DDT Exposure and Domoic Acid–Induced Seizures
The appearance of a chronic juvenile domoic acid disease in California sea lions is consistent with early life poisoning and may be potentiated by organochlorine burden. To investigate the interactive effect of DDT (diclorodiphenyltrichloroethane) on neurodevelopment, Tiedeken and Ramsdell (p. 68) used a zebrafish model for seizure behavior to examine susceptibility to domoic acid–induced seizures after completion of neurodevelopment. They found that embryonic exposure to DDTs led to asymptomatic animals with greater sensitivity to domoic acid–induced seizures. Their results suggest that p,p´-DDE may serve as an early developmental toxicant that enhances domoic acid poisoning of fetal California sea lions and the manifestation of chronic disease in juveniles.
BIOMONITORS | Development of a Biomarker of Wood Smoke Exposure
Biomass smoke is an important source of particulate matter. Short-term exposures to biomass smoke consist of periodic, seasonal exposures, whereas long-term exposures are typified by the use of biomass materials for cooking or heating. Levoglucosan (LG), a sugar anhydride released by combustion of cellulose-containing materials, is an attractive candidate biomarker of wood smoke exposure. Migliaccio et al. (p. 74) assessed LG in urine of Balb/c mice and children to determine its feasibility as a biomarker and found that LG was detectable in the urine of in wood smoke–exposed mice and humans, suggesting that it is a good candidate as a biomarker of exposure.
CARDIOVASCULAR DISEASE | Iron Metabolism Genes, Lead, and QT Interval
Cumulative exposure to lead is associated with depression of electrocardiographic conduction, such as prolonged QT interval. Because iron can enhance the oxidative effects of lead, Park et al. (p. 80) examined whether polymorphisms in iron metabolism genes [hemochromatosis (HFE), transferrin (TF) C2, and heme oxygenase-1 (HMOX-1)] increase susceptibility to the effects of lead on QT interval in 613 community-dwelling older men. Evidence suggests that gene variants related to iron metabolism increase the impact of low-level lead exposure on the prolonged QT interval.
EXPOSURE SCIENCE | Phthalate Metabolites in Lactating Women
Hines et al. (p. 86) measured and compared the concentrations of oxidative monoester phthalate metabolites in breast milk and surrogate fluids (serum, saliva, and urine) of 33 lactating North Carolina women. They also administered a questionnaire to determine routes of exposure. Phthalate metabolites were most frequently detected in urine of lactating women and less often detected in serum, milk, and saliva. Urinary phthalate concentrations reflected maternal exposure but did not represent the concentrations of oxidative metabolites in breast milk and other body fluids.
HUMAN TOXICOLOGY | Metabolites of PBDEs in Human Blood
Qiu et al. (p. 93) determined the concentrations of hydroxylated polybrominated diphenyl ethers (HO-PBDEs) in blood from pregnant women who had not been intentionally or occupationally exposed to these flame retardants, and from their newborn babies, and then compared these concentrations with those reported in mice. The PBDE metabolite pattern observed in humans differed from that in mice, indicating that different enzymes might be involved in the metabolic process. Levels of HO-PBDE metabolites were low but similar to parent compounds, which suggests that metabolites may accumulate in human blood.
NUTRITION | Dietary Intakes and Urinary Arsenic Excretion
In Bangladesh, millions of people are exposed to arsenic in their drinking water. Once ingested, arsenic is metabolized via methylation and excreted in urine. Heck et al. (p. 99) examined associations between intakes of protein, methionine, and cysteine with total urinary arsenic in a large population-based sample. Greater intakes were associated with 10–15% greater total urinary arsenic excretion, after controlling for energy intake, body weight, sex, age, tobacco use, and some other nutrients. Given previously reported associations between lower rates of arsenic excretion and increased rates of cancer, these findings support the role of nutrition in preventing arsenic-related disease.
CARDIOVASCULAR DISEASE | Effect Modifiers of PM2.5 Associated with HRV
de Hartog et al. (p. 105) evaluated whether exposure misclassification, effect modification by medication, or differences in particle composition could explain inconsistent associations between particulate matter < 2.5 µm in aerodynamic diameter (PM2.5) and heart rate variability (HRV). The results suggest that differences in the composition of particles, beta-blocker use, and obesity of study subjects may explain some inconsistencies among previous studies on HRV.
NEUROTOXICITY | Chlorpyrifos Alters Neuropeptide Expression
Evidence from animal and human studies indicates that chlorpyrifos (CPF), similar to other organophosphorus insecticides still widely used, is a developmental neurotoxicant. Developmental exposure to CPF in rodents induces sex-dimorphic behavioral changes at adulthood, which suggests that CPF may interfere with maturation of neuroendocrine mechanisms. Tait et al. (p. 112) investigated whether CPF affects levels of neurohypophyseal hormones that may modulate social behavior in mammals. Data indicate that developmental exposure to CPF may permanently interfere with specific key signaling proteins of the hypothalamic peptidergic system, with time-, dose-, and sex-related effects still evident at adulthood.
NEURODEGENERATIVE DISEASE | Parkinson’s Disease and the Environment
Parkinson’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. Bronstein et al. (p. 117) report on a multidisciplinary group of experts who gathered to assess what is known about the contribution of environmental factors to PD. PD is a complex disorder, and multiple different pathogenic pathways and mechanisms can ultimately lead to PD. Interplay among environmental factors and genetic makeup likely influences the risk of developing PD.
Children's Health
CHILD DEVELOPMENT | Childhood BMI and Environmental Pollution
Verhulst et al. (p. 122) investigated the association between body mass index (BMI) standard deviation score and prenatal exposure to hexachlorobenzene, dichlorodiphenyldichloroethylene (DDE), dioxin-like compounds, and polychlorinated biphenyls (PCBs) in a random sample of mother–infant pairs living in Flanders, Belgium. PCBs were associated with increased BMI during early childhood. Future studies are needed to confirm the findings and to assess possible mechanisms by which these pollutants could alter energy metabolism.
Also see Science Selections, p. A33
RISK ASSESSMENT | Air Pollution and Perinatal Mortality
Scientific evidence has correlated low birth weight and preterm birth—both important determinants of perinatal death—with air pollution. de Medeiros et al. (p. 127) examined the association between traffic-related pollution and perinatal mortality. Logistic regression revealed a gradient of increasing early neonatal death with higher exposure to traffic-related air pollution. Associations with fetal mortality were less consistent. The results suggest that motor vehicle exhaust exposures may be a risk factor for perinatal mortality.
RISK ASSESSMENT | Air Pollution and Perinatal Mortality
Scientific evidence has correlated low birth weight and preterm birth—both important determinants of perinatal death—with air pollution. de Medeiros et al. (p. 127) examined the association between traffic-related pollution and perinatal mortality. Logistic regression revealed a gradient of increasing early neonatal death with higher exposure to traffic-related air pollution. Associations with fetal mortality were less consistent. The results suggest that motor vehicle exhaust exposures may be a risk factor for perinatal mortality.
CANCER | Paint, Solvents, and the Risk of Childhood Leukemia
In this case–control study, Scélo et al. (p. 133) examined whether the use of paint and petroleum solvents at home before birth and in early childhood was associated with leukemia in children. The association between acute lymphoblastic leukemia and paint exposure was strong, but further studies are needed to confirm the association of acute lymphoblastic leukemia and acute myeloid leukemia risk with solvent exposure.
RESPIRATORY DISEASE | Air Pollution Exposure and Childhood Respiratory Allergies
Childhood respiratory allergies, which contribute to missed school days and other activity limitations, have increased in recent years, possibly due to environmental factors. Parker et al. (p. 140) examined whether air pollutants are associated with childhood respiratory allergies in the United States. For the approximately 70,000 children from the 1999–2005 National Health Interview Survey eligible for this study, the authors assigned ambient pollution monitoring data from the U.S. Environmental Protection Agency to 40,000–60,000, depending on the pollutant. The results provide evidence of adverse health for children living in areas with chronic exposure to higher levels of ozone and particulate matter < 2.5 µm in aerodynamic diameter compared with children with lower exposures.
EXPOSURE SCIENCE | Lead Carbonate as a Source of Lead in Children
In late 2006, the seaside community in Esperance, Western Australia, was alerted to thousands of native bird species dying from lead poisoning. The Pb was thought to derive from the handling and shipping of Pb carbonate concentrate from the Magellan mine, begun in July 2005. Gulson et al. (p. 148) evaluated the source of Pb in blood of a random sample of children and adults in the community. Isotopic data and mineralogic and particle size analyses indicated that, apart from the recognized pathway of Pb exposure by hand-to-mouth activity in children, the inhalation pathway could have been a significant contributor to PbB for some of the very young children and in some parents.