Environews
FOCUS | Linking TB and the Environment: An Overlooked Mitigation Strategy
Tuberculosis (TB) has been around almost as long as there have been humans to catch it. Today, evidence suggests that environmental risk factors, many arising from socioeconomic inequities, are contributing to the persistence and virulence of this disease around the globe. As drug-resistant strains begin to emerge and spread, researchers are faced with the task of developing more effective control measures to curb the spread of TB throughout vulnerable populations. This article (p. A478) discusses how environmental conditions can influence risk for TB and looks at how this understanding might be applied to controlling the disease.
SPHERES OF INFLUENCE | Oversight Without Obstruction: The Challenge for High-Containment Labs
The 2001 anthrax assaults through the postal system heightened awareness of U.S. vulnerability to attacks with biological weapons, a threat that has led to the planned building of a federal National Bio- and Agro-Defense Facility as well as broad expansion of high-containment laboratories to study a variety of hazardous pathogens. Many experts in microbiological research, while agreeing that these laboratories provide much-needed information, question how closely they are being monitored, as described in this article (p. A486)
Commentary
CARCINOGENESIS | Bioassay Protocols for Identifying Chemical Carcinogens
Chemical carcinogenesis bioassays in animals are accepted as valid predictors of potential cancer hazards to humans. In most rodent bioassays, animals are exposed to chemicals or other substances, including workplace and environmental pollutants, beginning at several weeks of age and continuing for 2 years. New findings indicate that the timing and duration of exposures used in rodent bioassays should be extended. Huff et al. (p. 1439) propose that the sensitivity of chemical carcinogenesis bioassays would be enhanced by exposing rodents in utero and continuing for 30 months (130 weeks) or until their natural deaths.
Review
RISK ASSESSMENT | Dioxins and Cardiovascular Disease Mortality
Humblet et al. (p. 1443) reviewed the evidence on the association between dioxin exposure and cardiovascular disease (CVD) mortality in humans. They conducted a PubMed search considering all English-language epidemiologic studies and their citations regarding dioxin exposure and CVD mortality. To focus on dioxins, they excluded cohorts that were either primarily exposed to polychlorinated biphenyls or that were from the leather and perfume industries, which include other cardiotoxic coexposures. Results suggest that dioxin exposure is associated with mortality from both ischemic heart disease and all CVD, although more strongly with ischemic heart disease. However, confounding by other CVD risk factors could not be determined.
Also see Science Selections, p. A491
CLIMATE CHANGE | Climate Change, Air Pollution, and Health Impacts
Because the state of the atmosphere determines the development, transport, dispersion, and deposition of air pollutants, there is concern that climate change could affect morbidity and mortality associated with elevated concentrations of these gases and fine particles. Ebi and McGregor (p. 1449) reviewed studies projecting the impacts of climate change on air quality and effects of these changes on human health. If improved models continue to project higher ozone concentrations with climate change, then reducing greenhouse gas emissions would enhance the health of current and future generations.
Research
METABOLISM | Early-Life Parathion Exposure
Organophosphate pesticides, usually considered developmental neurotoxicants, may also have lasting effects on metabolic function. Lassiter et al. (p. 1456) assessedthe impact of neonatal exposure to parathion, an organophosphate, on weight gain, food consumption, and glucose and lipid homeostasis, as well as the interaction with the effects of a high-fat diet in adult rats. Results show that neonatal low-dose parathion exposure disrupts glucose and fat homeostasis in a persistent and sex-selective manner, thus indicating that developmental exposure to organophosphates or other environmental chemicals may play a role in the increased incidence of obesity and diabetes.
Also see Science Selections, p. A491
CARDIOVASCULAR DISEASE | Traffic-Related Air Pollution and Coronary Heart Disease
Kan et al. (p. 1463) examined the association between long-term traffic exposure and incidence of fatal and nonfatal coronary heart disease (CHD) in a population-based prospective cohort study. Of 13,309 subjects, 976 developed CHD over an average of 13 years of follow-up. The risk was higher for residents living within 300 m of major roads than for those living farther away. Higher long-term exposure to traffic is associated with incidence of CHD, independent of other risk factors. These findings suggest that traffic-related air pollution can influence the development of disease in ostensibily healthy middle-age persons.
EXPOSURE SCIENCE | Secondhand Smoke Exposure in Hospitality Venues in Europe
In the last few years, some European countries have implemented smoking bans in hospitality venues. However, the levels of secondhand smoke (SHS) in workers of these venues could still be extremely high in most countries. In a cross-sectional study of 10 European cities, Lopez et al. (p. 1469) assessed exposure to SHS in 167 hospitality venues (58 discotheques and pubs, 82 restaurants and cafeterias, and 27 fast-food restaurants). They found that hospitality workers in Europe, especially those working is discotheques and pubs, are occupationally exposed to very high levels of SHS, which may cause serious health risks such as lung cancer and cardiovascular and respiratory diseases.
REPRODUCTIVE HEALTH | Metals and Semen Quality
To assess relationships between exposure to multiple metals at environmental levels and human semen-quality parameters, Meeker et al. (p. 1473) measured semen quality (sperm concentration, motile sperm, and sperm morphology) and metals in blood from 219 men recruited through two infertility clinics. They found dose-dependent trends between molybdenum, a ubiquitous trace element found in food and drinking water and present in multivitamin/multimineral supplements, and reduced sperm concentration and normal morphology, even when considering potential confounders and other metals.
RISK ASSESSMENT | Effects of Particulate Matter on Mortality
Samoli et al. (p. 1480) evaluated the findings of the APHENA (Air Pollution and Health: A Combined European and North American Approach) study, a collaborative analysis of multicity time-series data on the effect of air pollution on population health. The authors used Poisson regression models, with natural and penalized splines, to adjust for seasonality, and then used meta-regression approaches to combine time-series results across cites and to assess effect modification by selected ecologic covariates. Results show the effects of PM10 (particulate matter ≤ 10 µm in aerodynamic diameter) on the daily number of deaths for all ages and for those < 75 and ≥ 75 years of age.
RESPIRATORY DISEASE | Nasal Immune Response to DEHP in Allergic Subjects
Deutschle et al. (p. 1487) investigated the effects of house dust containing di(2-ethylhexyl) phthalate (DEHP) on nasal mucosa of healthy and house dust mite (HDM)–allergic subjects in a short-term exposure setting. The authors found that nasal exposure to house dust with low or high DEHP concentrations had no effect on symptom scores. Although healthy subjects had almost no response to inhaled dust, HDM-allergic subjects showed varied responses. Results suggest that short-term exposure to high concentrations of DEHP in house dust has attenuating effects on human nasal immune response in HDM-allergic subjects, involving both gene expression and cytokines.
Also see Science Selections, p. A490
GENE POLYMORPHISM | GST Polymorphisms and Heart Rate Variability
Disturbances in heart rate variability (HRV) may represent one pathway by which second-hand smoke (SHS) and air pollutants affect cardiovascular morbidity and mortality. However, the mechanisms are poorly understood. Probst-Hensch et al. (p. 1494) investigated the hypothesis that oxidative stress alters cardiac autonomic control by studying the association of polymorphisms in oxidant-scavenging glutathione S-transferase (GST) genes and their interactions with HRV, SHS, and obesity. They found that GST deficiency is associated with significant HRV alterations in the general population. Their results are consistent with an impact of oxidative stress on the autonomous nervous system.
ASTHMA | Lung Responses to Ambient Particulate Matter in a Murine Asthma Model
Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Exposures to environmental factors such as ambient particulate matter (PM) contribute to increased asthma prevalence and exacerbations. Wang et al. (p. 1500) investigated pathophysiologic responses to ambient Baltimore, Maryland, PM in a murine model of asthma and attempted to identify PM-specific genomic/molecular signatures. This study is consistent with emerging epidemiologic evidence. Results indicate that PM exposure evokes proinflammatory and allergic molecular signatures that may directly contribute to the asthma susceptibility in naive subjects and increased severity in affected asthmatics.
EXPOSURE SCIENCE | Prenatal Exposure to Airborne Polycyclic Aromatic Hydrocarbons
In a cohort of pregnant women in Krakow, Poland, Choi et al. (p. 1509) examined the contribution of temporal, spatial, and behavioral factors to prenatal exposure to airborne PAHs within each trimester and developed a predictive model of PAH exposure over the entire gestational period. The use of cross-sectional, longitudinal monitoring supplemented with questionnaire data allowed development of a gestation-length model of individual-level exposure with high precision and validity.
Also see Science Selections, p. A490
GENE EXPRESSION | Transcriptome Analysis in Human Blood as a Biomarker
Human carcinogenesis is initiated and/or promoted by exposure to chemicals that occur in the environment. Molecular cancer epidemiology is used to identify human environmental cancer risks by applying a range of effect biomarkers. Toxicogenomic technologies may offer improvements by providing the opportunity to identify molecular biomarkers consisting of altered gene expression profiles. van Leeuwen et al. (p. 1519) monitored the expression of selected genes in a random sample of adults in Flanders selected from specific regions with (presumably) different environmental burdens. Gene expression profiling appears promising as a tool for biological monitoring in relation to environmental exposures in humans.
REPRODUCTIVE HEALTH | Gonadal Abnormalities Are Associated with Agriculture
Evidence of endocrine disruption in wild amphibians living in agricultural areas remains controversial, and most studies on the effects of pollutants on wildlife attempt to compare polluted sites with unpolluted sites. To investigate this issue, McCoy et al. (p. 1526) quantified the relationship between gonadal abnormalities and habitats characterized by differing degrees of agricultural activity. They found that the number of abnormalities and frequency of intersex gonads increased with agriculture in a dose-dependent fashion and that these gonadal abnormalities were associated with altered gonadal function. These reproductive abnormalities occurring in areas exposed to agricultural contaminants could contribute to amphibian population declines.
POPULATION HEALTH | Drinking Water Quality during Storage in Ecuador
In a rural setting in northern coastal Ecuador, Levy et al. (p. 1533) sampled source waters concurrently with water collected by household members and followed this water over time, comparing Escherichia coli and enterococci concentrations in water stored in households with water stored under controlled conditions. They found that water quality improved after water was transferred from the source to household storage containers, but then declined because of recontamination in the home. These results will be helpful in designing interventions to improve water quality and supply, even for those who rely primarily on unimproved surface sources of drinking water.
CANCER | Cancer Incidence in a Cohort of EPTC Applicators
The U.S. Environmental Protection Agency has reported that EPTC (S-ethyl-N,N-dipropylthiocarbamate), a thiocarbamate herbicide used in every region of the United States, is most likely not a human carcinogen; however, epidemiologic data on EPTC exposure and cancer risk are scarce. Using data from the Agricultural Health Study (AHS), a prospective cohort study of licensed pesticide applicators from Iowa and North Carolina enrolled between 1993 and 1997, van Bemmel et al. (p. 1541) examined cancer incidence and EPTC use in 48,378 male pesticide applicators. Results showed that, in this population, EPTC use appeared to be associated with colon cancer and leukemia.
GENE EXPRESSION | Global DNA Hypomethylation Associated with Serum POPs
Persistent organic pollutants (POPs) may influence epigenetic mechanisms; that is, they could affect chromosomal stability and gene expression. DNA methylation, an epigenetic mechanism, has been associated with cancer initiation and progression. Using blood samples collected under the Arctic Monitoring and Assessment Program and previously analyzed for a battery of POPs, Rusiecki et al. (p. 1547) evaluated the relationship between plasma POP concentrations and global DNA methylation (percent 5-methylcytosine) in DNA extracted from blood samples from 70 Greenlandic Inuit. Global methylation levels were inversely associated with blood plasma levels for several POPs. These results support the hypothesis that exposure to potentially carcinogenic compounds such as POPs may influence DNA methylation.
LIVER | Aflatoxin in Etiology of Cirrhosis in West Africa
Because cirrhosis of the liver is thought to be a major cause of morbidity and mortality in sub-Saharan Africa, Kuniholm et al. (p. 1553) explored the association between environmental and infectious exposures and cirrhosis in The Gambia. Study participants (97 who were diagnosed with cirrhosis and 397 controls) reported demographic and food frequency information. Blood samples were tested for hepatitis B surface antigen, hepatitis B e antigen, hepatitis C virus (HCV) antibody, HCV RNA, and the aflatoxin-associated 249ser TP53 mutation. Results suggest that the spectrum of morbidity associated with aflatoxin exposure could include cirrhosis.
DENTAL HEALTH | Persistent Organic Pollutants and Periodontitiss
Persistent organic pollutants (POPs), which are endocrine disruptors that accumulate in adipose tissue, can increase the risk of periodontal disease through the disturbance of the immune system. Lee et al. (p. 1558) examined associations of background exposure to POPs with periodontal disease in the general population. They investigated cross-sectional associations of concentrations of serum POPs with the prevalence of periodontal disease in 1,234 adults ≥ 20 years of age in the National Health and Nutrition Examination Survey 1999–2002. POPs, especially organochlorine (OC) pesticides, were positively associated with periodontal disease, possibly through immunomodulation due to OC pesticides.
ENVIRONMENTAL TOXICOLOGY | Assessment of Tamiflu Release to the Environment
Singer et al. (p. 1563) report on the workshop Tamiflu and the Environment: Implications of Use under Pandemic Conditions, which was organized to assess the potential human health impact and environmental hazards associated with use of Tamiflu during an influenza pandemic. The consensus of workshop participants was that oseltamivir ethylester-phosphate and oseltamivir carboxylate (OC) were unlikely to pose an ecotoxicologic hazard to freshwater organisms. OC in river water might hasten the generation of OC-resistance in wildfowl, but this possibility was seems less likely than the potential disruption that OC and other pharmaceuticals could pose to the operation of sewage treatment plants.
HUMAN TOXICOLOGY | Upstream Adverse End Points
Assessing adverse effects from environmental chemical exposure is integral to public health policies. Toxicology assays identifying early biological changes from chemical exposure are increasing our ability to evaluate links between early biological disturbances and subsequent overt downstream effects. Woodruff et al. (p. 1568) report on a workshop held to consider how the resulting data inform consideration of an "adverse effect" in the context of hazard identification and risk assessment. The authors review what is known about the relationships between chemical exposure, early biological effects (upstream events), and later overt effects (downstream events) through three case studies, and they discuss how to evaluate hazard and risk when early biological effect data are available.
Children's Health
CANCER | Hazardous Air Pollutants and Childhood Cancer
Cancer is the second leading cause of death among U.S. children with few known risk factors. There is increasing interest in the role of air pollutants, including benzene and 1,3-butadiene, in the etiology of childhood cancers. Whitworth et al. (p. 1576) investigated whether census tracts with the highest benzene or 1,3-butadiene ambient air levels have increased childhood lymphohematopoietic cancer incidence. They analyzed 977 cases of childhood lymphohematopoietic cancer diagnosed from 1995 to 2004 in 886 census tracts surrounding Houston, Texas. Results of their ecologic analysis suggest an association between childhood leukemia and hazardous air pollution.
NEURODEVELOPMENT | GST Genes, DDT, and Neurodevelopment at 4 Years of Age
Early-life exposure to DDT (2,2-bis[p-chlorophenyl]-1,1,1-trichloroethane) is associated with a decrease in cognitive skills among preschoolers at 4 years of age. Morales et al. (p. 1581) hypothesized that genetic variability in glutathione S-transferase (GST) genes (GSTP1, GSTM1, and GSTT1) could influence the effects of prenatal exposure to DDT. The cord serum concentration of DDT was inversely associated with general cognitive, memory, quantitative, and verbal skills, as well as with executive function and working memory, in children who had any GSTP1 Val-105 allele. Results indicate that children with the GSTP1 Val-105 allele were at higher risk of the adverse cognitive functioning effects of prenatal DDT exposure.
FETAL/CHILD DEVELOPMENT | Prenatal Lead and Schizophrenia
A previous study of prenatal lead exposure and schizophrenia in archived maternal serum samples collected from subjects enrolled in the Childhood Health and Development Study (1959–1966) suggested a possible association between prenatal Pb exposure and the development of schizophrenia later in life. Opler et al. (p. 1586) used samples collected from the New England cohort of the National Collaborative Perinatal Project (1959–1966) to extend these findings. Although several limitations constrain generalizability, the results are consistent with previous findings and provide further evidence for the role of early environmental exposures in the development of adult-onset psychiatric disorders.
