What’s in the Pool? A Comprehensive Identification of Disinfection By-products and Assessment of Mutagenicity of Chlorinated and Brominated Swimming Pool Water

Background

Swimming pool disinfectants and disinfection by-products (DBPs) have been linked to human health effects, including asthma and bladder cancer, but no studies have provided a comprehensive identification of DBPs in the water and related that to mutagenicity.

Objectives

We performed a comprehensive identification of DBPs and disinfectant species in waters from public swimming pools in Barcelona, Catalonia, Spain, that disinfect with either chlorine or bromine and we determined the mutagenicity of the waters to compare with the analytical results.

Methods

We used gas chromatography/mass spectrometry (GC/MS) to measure trihalomethanes in water, GC with electron capture detection for air, low- and high-resolution GC/MS to comprehensively identify DBPs, photometry to measure disinfectant species (free chlorine, monochloroamine, dichloramine, and trichloramine) in the waters, and an ion chromatography method to measure trichloramine in air. We assessed mutagenicity with the Salmonella mutagenicity assay.

Results

We identified > 100 DBPs, including many nitrogen-containing DBPs that were likely formed from nitrogen-containing precursors from human inputs, such as urine, sweat, and skin cells. Many DBPs were new and have not been reported previously in either swimming pool or drinking waters. Bromoform levels were greater in brominated than in chlorinated pool waters, but we also identified many brominated DBPs in the chlorinated waters. The pool waters were mutagenic at levels similar to that of drinking water (~ 1,200 revertants/L-equivalents in strain TA100–S9 mix).

Conclusions

This study identified many new DBPs not identified previously in swimming pool or drinking water and found that swimming pool waters are as mutagenic as typical drinking waters.     

Genotoxic Effects in Swimmers Exposed to Disinfection By-products in Indoor Swimming Pools

Background

Exposure to disinfection by-products (DBPs) in drinking water has been associated with cancer risk. A recent study (Villanueva et al. 2007; Am J Epidemiol 165:148–156) found an increased bladder cancer risk among subjects attending swimming pools relative to those not attending.

Objectives

We evaluated adults who swam in chlorinated pools to determine whether exposure to DBPs in pool water is associated with biomarkers of genotoxicity.

Methods

We collected blood, urine, and exhaled air samples from 49 nonsmoking adult volunteers before and after they swam for 40 min in an indoor chlorinated pool. We estimated associations between the concentrations of four trihalomethanes (THMs) in exhaled breath and changes in micronuclei (MN) and DNA damage (comet assay) in peripheral blood lymphocytes before and 1 hr after swimming; urine mutagenicity (Ames assay) before and 2 hr after swimming; and MN in exfoliated urothelial cells before and 2 weeks after swimming. We also estimated associations and interactions with polymorphisms in genes related to DNA repair or to DBP metabolism.

Results

After swimming, the total concentration of the four THMs in exhaled breath was seven times higher than before swimming. The change in the frequency of micronucleated lymphocytes after swimming increased in association with higher exhaled concentrations of the brominated THMs (p = 0.03 for bromodichloromethane, p = 0.05 for chlorodibromomethane, p = 0.01 for bromoform) but not chloroform. Swimming was not associated with DNA damage detectable by the comet assay. Urine mutagenicity increased significantly after swimming, in association with the higher concentration of exhaled bromoform (p = 0.004). We found no significant associations with changes in micronucleated urothelial cells.

Conclusions

Our findings support potential genotoxic effects of exposure to DBPs from swimming pools. The positive health effects gained by swimming could be increased by reducing the potential health risks of pool water.     

Short-Term Changes in Respiratory Biomarkers after Swimming in a Chlorinated Pool

Background

Swimming in chlorinated pools involves exposure to disinfection by-products (DBPs) and has been associated with impaired respiratory health.

Objectives

We evaluated short-term changes in several respiratory biomarkers to explore mechanisms of potential lung damage related to swimming pool exposure.

Methods

We measured lung function and biomarkers of airway inflammation [fractional exhaled nitric oxide (FeNO), eight cytokines, and vascular endothelial growth factor (VEGF) in exhaled breath condensate], oxidative stress (8-isoprostane in exhaled breath condensate), and lung permeability [surfactant protein D (SP-D) and the Clara cell secretory protein (CC16) in serum] in 48 healthy nonsmoking adults before and after they swam for 40 min in a chlorinated indoor swimming pool. We measured trihalomethanes in exhaled breath as a marker of individual exposure to DBPs. Energy expenditure during swimming, atopy, and CC16 genotype (rs3741240) were also determined.

Results

Median serum CC16 levels increased from 6.01 to 6.21 μg/L (average increase, 3.3%; paired Wilcoxon test p = 0.03), regardless of atopic status and CC16 genotype. This increase was explained both by energy expenditure and different markers of DBP exposure in multivariate models. FeNO was unchanged overall but tended to decrease among atopics. We found no significant changes in lung function, SP-D, 8-isoprostane, eight cytokines, or VEGF.

Conclusions

We detected a slight increase in serum CC16, a marker of lung epithelium permeability, in healthy adults after they swam in an indoor chlorinated pool. Exercise and DBP exposure explained this association, without involving inflammatory mechanisms. Further research is needed to confirm the results, establish the clinical relevance of short-term serum CC16 changes, and evaluate the long-term health impacts.     

Ecological association between childhood asthma and availability of indoor chlorinated swimming pools in Europe

Background

It has been hypothesised that the rise in childhood asthma in the developed world could result at least in part from the increasing exposure of children to toxic chlorination products in the air of indoor swimming pools.

Objectives

Ecological study to evaluate whether this hypothesis can explain the geographical variation in the prevalence of asthma and other atopic diseases in Europe.

Methods

The relationships between the prevalences of wheezing by written or video questionnaire, of ever asthma, hay fever, rhinitis, and atopic eczema as reported by the International Study of Asthma and Allergies in Childhood (ISAAC), and the number of indoor chlorinated swimming pools per inhabitant in the studied centres were examined. Associations with geoclimatic variables, the gross domestic product (GDP) per capita, and several other lifestyle indicators were also evaluated.

Results

Among children aged 13–14 years, the prevalence of wheezing by written questionnaire, of wheezing by video questionnaire, and of ever asthma across Europe increased respectively by 3.39% (95% CI 1.96 to 4.81), 0.96% (95% CI 0.28 to 1.64), and 2.73% (95% CI 1.94 to 3.52), with an increase of one indoor chlorinated pool per 100 000 inhabitants. Similar increases were found when analysing separately centres in Western or Northern Europe and for ever asthma in Southern Europe. In children aged 6–7 years (33 centres), the prevalence of ever asthma also increased with swimming pool availability (1.47%; 95% CI 0.21 to 2.74). These consistent associations were not found with other atopic diseases and were independent of the influence of altitude, climate, and GDP per capita.

Conclusions

The prevalence of childhood asthma and availability of indoor swimming pools in Europe are linked through associations that are consistent with the hypothesis implicating pool chlorine in the rise of childhood asthma in industrialised countries.     

Childhood Incident Asthma and Traffic-Related Air Pollution at Home and School

Background

Traffic-related air pollution has been associated with adverse cardiorespiratory effects, including increased asthma prevalence. However, there has been little study of effects of traffic exposure at school on new-onset asthma.

Objectives

We evaluated the relationship of new-onset asthma with traffic-related pollution near homes and schools.

Methods

Parent-reported physician diagnosis of new-onset asthma (n = 120) was identified during 3 years of follow-up of a cohort of 2,497 kindergarten and first-grade children who were asthma- and wheezing-free at study entry into the Southern California Children’s Health Study. We assessed traffic-related pollution exposure based on a line source dispersion model of traffic volume, distance from home and school, and local meteorology. Regional ambient ozone, nitrogen dioxide (NO₂), and particulate matter were measured continuously at one central site monitor in each of 13 study communities. Hazard ratios (HRs) for new-onset asthma were scaled to the range of ambient central site pollutants and to the residential interquartile range for each traffic exposure metric.

Results

Asthma risk increased with modeled traffic-related pollution exposure from roadways near homes [HR 1.51; 95% confidence interval (CI), 1.25–1.82] and near schools (HR 1.45; 95% CI, 1.06–1.98). Ambient NO₂ measured at a central site in each community was also associated with increased risk (HR 2.18; 95% CI, 1.18–4.01). In models with both NO₂ and modeled traffic exposures, there were independent associations of asthma with traffic-related pollution at school and home, whereas the estimate for NO₂ was attenuated (HR 1.37; 95% CI, 0.69–2.71).

Conclusions

Traffic-related pollution exposure at school and homes may both contribute to the development of asthma.     

Chronic Exposure to Ambient Ozone and Asthma Hospital Admissions among Children

Background

The association between chronic exposure to air pollution and adverse health outcomes has not been well studied.

Objective

This project investigated the impact of chronic exposure to high ozone levels on childhood asthma admissions in New York State.

Methods

We followed a birth cohort born in New York State during 1995–1999 to first asthma admission or until 31 December 2000. We identified births and asthma admissions through the New York State Integrated Child Health Information System and linked these data with ambient ozone data (8-hr maximum) from the New York State Department of Environmental Conservation. We defined chronic ozone exposure using three indicators: mean concentration during the follow-up period, mean concentration during the ozone season, and proportion of follow-up days with ozone levels > 70 ppb. We performed logistic regression analysis to adjust for child’s age, sex, birth weight, and gestational age; maternal race/ethnicity, age, education, insurance status, smoking during pregnancy, and poverty level; and geographic region, temperature, and copollutants.

Results

Asthma admissions were significantly associated with increased ozone levels for all chronic exposure indicators (odds ratios, 1.16–1.68), with a positive dose–response relationship. We found stronger associations among younger children, low sociodemographic groups, and New York City residents as effect modifiers.

Conclusion

Chronic exposure to ambient ozone may increase the risk of asthma admissions among children. Younger children and those in low socioeconomic groups have a greater risk of asthma than do other children at the same ozone level.     

Ten Years of Addressing Children’s Health through Regulatory Policy at the U.S. Environmental Protection Agency

Background

Executive Order (EO) 13045, Protection of Children From Environmental Health Risks and Safety Risks, directs each federal agency to ensure that its policies, programs, activities, and standards address disproportionate environmental health and safety risks to children.

Objectives

We reviewed regulatory actions published by U.S. Environmental Protection Agency (EPA) in the Federal Register from April 1998 through December 2006 to evaluate applicability of EO 13045 to U.S. EPA actions and consideration of children’s health issues in U.S. EPA rulemakings.

Discussion

Although virtually all actions discussed EO 13045, fewer than two regulations per year, on average, were subject to the EO requirement to evaluate children’s environmental health risks. Nonetheless, U.S. EPA considered children’s environmental health in all actions addressing health or safety risks that may disproportionately affect children.

Conclusion

The EO does not apply to a broad enough set of regulatory actions to ensure protection of children’s health and safety risks, largely because of the small number of rules that are economically significant. However, given the large number of regulations that consider children’s health issues despite not being subject to the EO, other statutory requirements and agency policies reach a larger set of regulations to ensure protection of children’s environmental health.     

Chlorination Disinfection By-Products in Drinking Water and Congenital Anomalies: Review and Meta-Analyses

Objectives

The aim of this study was to review epidemiologic evidence, provide summary risk estimates of the association between exposure to chlorination disinfection by-products (DBPs) and congenital anomalies, and provide recommendations for future studies.

Data sources and extraction

We included all published epidemiologic studies that evaluated a relationship between an index of DBP exposure (treatment, water source, DBP measurements, and both DBP measurements and personal characteristics) and risk of congenital anomalies. When three or more studies examined the same exposure index and congenital anomaly, we conducted a meta-analysis to obtain a summary risk estimate comparing the highest exposure group with the lowest exposure group. When five or more studies examined total trihalomethane (TTHM) exposure and a specific congenital anomaly, we conducted a meta-analysis to obtain exposure–response risk estimates per 10 μg/L TTHM.

Data synthesis

For all congenital anomalies combined, the meta-analysis gave a statistically significant excess risk for high versus low exposure to water chlorination or TTHM [17%; 95% confidence interval (CI), 3–34] based on a small number of studies. The meta-analysis also suggested a statistically significant excess risk for ventricular septal defects (58%; 95% CI, 21–107), but this was based on only three studies, and there was little evidence of an exposure–response relationship. We observed no statistically significant relationships in the other meta-analyses. We found little evidence for publication bias, except for urinary tract defects and cleft lip and palate.

Conclusion

Although some individual studies have suggested an association between chlorination disinfection by-products and congenital anomalies, meta-analyses of all currently available studies demonstrate little evidence of such an association.     

Exposure assessment in cohort studies of childhood asthma

Background

The environment is suspected to play an important role in the development of childhood asthma. Cohort studies are a powerful observational design for studying exposure–response relationships, but their power depends in part upon the accuracy of the exposure assessment.

Objective

The purpose of this paper is to summarize and discuss issues that make accurate exposure assessment a challenge and to suggest strategies for improving exposure assessment in longitudinal cohort studies of childhood asthma and allergies.

Data synthesis

Exposures of interest need to be prioritized, because a single study cannot measure all potentially relevant exposures. Hypotheses need to be based on proposed mechanisms, critical time windows for effects, prior knowledge of physical, physiologic, and immunologic development, as well as genetic pathways potentially influenced by the exposures. Modifiable exposures are most important from the public health perspective. Given the interest in evaluating gene–environment interactions, large cohort sizes are required, and planning for data pooling across independent studies is critical. Collection of additional samples, possibly through subject participation, will permit secondary analyses. Models combining air quality, environmental, and dose data provide exposure estimates across large cohorts but can still be improved.

Conclusions

Exposure is best characterized through a combination of information sources. Improving exposure assessment is critical for reducing measurement error and increasing power, which increase confidence in characterization of children at risk, leading to improved health outcomes.     

Allergy and Sensitization during Childhood Associated with Prenatal and Lactational Exposure to Marine Pollutants

Background

Breast-feeding may affect the risk of developing allergy during childhood and may also cause exposure to immunotoxicants, such as polychlorinated biphenyls (PCBs), which are of concern as marine pollutants in the Faroe Islands and the Arctic region.

Objectives

The objective was to assess whether sensitization and development of allergic disease is associated with duration of breast-feeding and prenatal or postnatal exposures to PCBs and methylmercury.

Methods

A cohort of 656 singleton births was formed in the Faroe Islands during 1999–2001. Duration of breast-feeding and history of asthma and atopic dermatitis were recorded at clinical examinations at 5 and 7 years of age. PCB and mercury concentrations were determined in blood samples obtained at parturition and at follow-up. Serum from 464 children (71%) at 7 years of age was analyzed for total immunoglobulin E (IgE) and grass-specific IgE.

Results

The total IgE concentration in serum at 7 years of age was positively associated both with the concomitant serum PCB concentration and with the duration of breast-feeding. However, the effect only of the latter was substantially attenuated in a multivariate analysis. A raised grass-specific IgE concentration compatible with sensitization was positively associated with the duration of breast-feeding and inversely associated with prenatal methylmercury exposure. However, a history of asthma or atopic dermatitis was not associated with the duration of breast-feeding, although children with atopic dermatitis had lower prenatal PCB exposures than did nonallergic children.

Conclusions

These findings suggest that developmental exposure to immunotoxicants may both increase and decrease the risk of allergic disease and that associations between breast-feeding and subsequent allergic disease in children may, at least in part, reflect lactational exposure to immunotoxic food contaminants.     

Intellectual Impairment in School-Age Children Exposed to Manganese from Drinking Water

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 Relationship of Housing and Population Health: A 30-Year Retrospective Analysis

Objective

We analyzed the relationship between health status and housing quality over time.

Methods

We combined data from two nationally representative longitudinal surveys of the U.S. population and its housing, the National Health and Nutrition Examination Survey and the American Housing Survey, respectively. We identified housing and health trends from approximately 1970 to 2000, after excluding those trends for which data were missing or where we found no plausible association or change in trend.

Results

Changes in housing include construction type, proportion of rental versus home ownership, age, density, size, moisture, pests, broken windows, ventilation and air conditioning, and water leaks. Changes in health measures include asthma, respiratory illness, obesity and diabetes, and lead poisoning, among others. The results suggest ecologic trends in childhood lead poisoning follow housing age, water leaks, and ventilation; asthma follows ventilation, windows, and age; overweight trends follow ventilation; blood pressure trends follow community measures; and health disparities have not changed greatly.

Conclusions

Housing trends are consistent with certain health trends over time. Future national longitudinal surveys should include health, housing, and community metrics within a single integrated design, instead of separate surveys, in order to develop reliable indicators of how housing changes affect population health and how to best target resources. Little progress has been made in reducing the health and housing disparities of disadvantaged groups, with the notable exception of childhood lead poisoning caused by exposure to lead-based paint hazards. Use of these and other data sets to create reliable integrated indicators of health and housing quality are needed.     

Polymorphisms in GSTT1, GSTZ1, and CYP2E1, Disinfection By-products,and Risk of Bladder Cancer in Spain

Background

Bladder cancer has been linked with long-term exposure to disinfection by-products (DBPs) in drinking water.

Objectives

In this study we investigated the combined influence of DBP exposure and polymorphisms in glutathione S-transferase (GSTT1, GSTZ1) and cytochrome P450 (CYP2E1) genes in the metabolic pathways of selected by-products on bladder cancer in a hospital-based case–control study in Spain.

Methods

Average exposures to trihalomethanes (THMs; a surrogate for DBPs) from 15 years of age were estimated for each subject based on residential history and information on municipal water sources among 680 cases and 714 controls. We estimated effects of THMs and GSTT1, GSTZ1, and CYP2E1 polymorphisms on bladder cancer using adjusted logistic regression models with and without interaction terms.

Results

THM exposure was positively associated with bladder cancer: adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were 1.2 (0.8–1.8), 1.8 (1.1–2.9), and 1.8 (0.9–3.5) for THM quartiles 2, 3, and 4, respectively, relative to quartile 1. Associations between THMs and bladder cancer were stronger among subjects who were GSTT1 +/+ or +/− versus GSTT1 null (p_interaction = 0.021), GSTZ1 rs1046428 CT/TT versus CC (p_interaction = 0.018), or CYP2E1 rs2031920 CC versus CT/TT (p_interaction = 0.035). Among the 195 cases and 192 controls with high-risk forms of GSTT1 and GSTZ1, the ORs for quartiles 2, 3, and 4 of THMs were 1.5 (0.7–3.5), 3.4 (1.4–8.2), and 5.9 (1.8–19.0), respectively.

Conclusions

Polymorphisms in key metabolizing enzymes modified DBP-associated bladder cancer risk. The consistency of these findings with experimental observations of GSTT1, GSTZ1, and CYP2E1 activity strengthens the hypothesis that DBPs cause bladder cancer and suggests possible mechanisms as well as the classes of compounds likely to be implicated.     

Respiratory and allergic health effects of dampness, mold, and dampness-related agents: a review of the epidemiologic evidence

Objectives

Many 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 microbiologic factors have received little review. We conducted an updated, comprehensive review on these topics.

Data sources

We reviewed eligible peer-reviewed epidemiologic studies or quantitative meta-analyses, up to late 2009, on dampness, mold, or other microbiologic agents and respiratory or allergic effects.

Data extraction

We evaluated evidence for causation or association between qualitative/subjective assessments of dampness or mold (considered together) and specific health outcomes. We separately considered evidence for associations between specific quantitative measurements of microbiologic factors and each health outcome.

Data synthesis

Evidence from epidemiologic studies and meta-analyses showed indoor dampness or mold to be associated consistently with increased asthma development and exacerbation, current and ever diagnosis of asthma, dyspnea, wheeze, cough, respiratory infections, bronchitis, allergic rhinitis, eczema, and upper respiratory tract symptoms. Associations were found in allergic and nonallergic individuals. Evidence strongly suggested causation of asthma exacerbation in children. Suggestive evidence was available for only a few specific measured microbiologic factors and was in part equivocal, suggesting both adverse and protective associations with health.

Conclusions

Evident dampness or mold had consistent positive associations with multiple allergic and respiratory effects. Measured microbiologic agents in dust had limited suggestive associations, including both positive and negative associations for some agents. Thus, 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.     

Long-Term Traffic-Related Exposures and Asthma Onset in Schoolchildren in Oslo,Norway

Background

Whether there is a causal relation between long-term exposure to traffic and asthma development is so far not clear. This may be explained by inaccurate exposure assessment.

Objective

We investigated the associations of long-term traffic-related exposures with asthma onset assessed retrospectively and respiratory symptoms in 9- to 10-year-old children.

Methods

We collected information on respiratory outcomes and potential confounding variables by parental questionnaire in 2,871 children in Oslo. Nitrogen dioxide exposure was assessed by the EPISODE dispersion model and assigned at updated individual addresses during lifetime. Distance to major road was assigned at birth address and address by date of questionnaire. Cox proportional hazard regression and logistic regression were used.

Results

We did not find positive associations between any long-term traffic-related exposure and onset of doctor-diagnosed asthma. An interquartile range (IQR) increase of NO₂ exposure before asthma onset was associated with an adjusted risk ratio of 0.82 [95% confidence interval (CI), 0.67–1.02]. Handling early asthma cases (children < 4 years of age) with recovery during follow-up as noncases gave a less negative association. The associations for late asthma onset (≥ 4 years of age) were positive but not statistically significant. For current symptoms, an IQR increase of previous year’s NO₂ exposure was associated with adjusted odds ratios of 1.01 (95% CI, 0.83–1.23) for wheeze, 1.10 (95% CI, 0.79–1.51) for severe wheeze, and 1.01 (95% CI, 0.84–1.21) for dry cough.

Conclusions

We were not able to find positive associations of long-term traffic-related exposures with asthma onset or with current respiratory symptoms in 9- to 10-year-old children in Oslo.     

Murine Lung Responses to Ambient Particulate Matter: Genomic Analysis and Influence on Airway Hyperresponsiveness

Background

Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Epidemiologic studies have demonstrated that exposures to environmental factors such as ambient particulate matter (PM), a major air pollutant, contribute to increased asthma prevalence and exacerbations.

Objective

We investigated pathophysiologic responses to Baltimore, Maryland, ambient PM (median diameter, 1.78 μm) in a murine model of asthma and attempted to identify PM-specific genomic/molecular signatures.

Methods

We exposed ovalbumin (OVA)-sensitized A/J mice intratracheally to PM (20 mg/kg), and assayed both AHR and bronchoalveolar lavage (BAL) on days 1, 4, and 7 after PM exposure. Lung gene expression profiling was analyzed in OVA- and PM-challenged mice.

Results

Consistent with this murine model of asthma, we observed significant increases in airway responsiveness in OVA-treated mice, with PM exposure inducing significant changes in AHR in both naive mice and OVA-induced asthmatic mice. PM evoked eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of type 1 T helper (T_H1) cytokines [interferon-γ, interleukin-6 (IL-6), tumor necrosis factor-α] and T_H2 cytokines (IL-4, IL-5, eotaxin) into murine airways. Furthermore, PM consistently induced expression of genes involved in innate immune responses, chemotaxis, and complement system pathways.

Conclusion

This study is consistent with emerging epidemiologic evidence and indicates 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.     

A Framework for Widespread Replication of a Highly Spatially Resolved Childhood Lead Exposure Risk Model

Background

Preventive approaches to childhood lead poisoning are critical for addressing this longstanding environmental health concern. Moreover, increasing evidence of cognitive effects of blood lead levels < 10 μg/dL highlights the need for improved exposure prevention interventions.

Objectives

Geographic information system–based childhood lead exposure risk models, especially if executed at highly resolved spatial scales, can help identify children most at risk of lead exposure, as well as prioritize and direct housing and health-protective intervention programs. However, developing highly resolved spatial data requires labor-and time-intensive geocoding and analytical processes. In this study we evaluated the benefit of increased effort spent geocoding in terms of improved performance of lead exposure risk models.

Methods

We constructed three childhood lead exposure risk models based on established methods but using different levels of geocoded data from blood lead surveillance, county tax assessors, and the 2000 U.S. Census for 18 counties in North Carolina. We used the results to predict lead exposure risk levels mapped at the individual tax parcel unit.

Results

The models performed well enough to identify high-risk areas for targeted intervention, even with a relatively low level of effort on geocoding.

Conclusions

This study demonstrates the feasibility of widespread replication of highly spatially resolved childhood lead exposure risk models. The models guide resource-constrained local health and housing departments and community-based organizations on how best to expend their efforts in preventing and mitigating lead exposure risk in their communities.     

Proton magnetic resonance spectroscopy in adults with childhood lead exposure

Background

Childhood lead exposure adversely affects neurodevelopment. However, few studies have examined changes in human brain metabolism that may underlie known adverse cognitive and behavioral outcomes.

Objective

We examined the association between mean childhood blood lead levels and in vivo brain metabolite concentrations as adults, determined by proton magnetic resonance spectroscopy (MRS) in a birth cohort with documented low-to-moderate lead exposure.

Methods

Adult participants from the Cincinnati Lead Study [n = 159; mean age (± SD), 20.8 ± 0.9 years] completed a quantitative, short-echo proton MRS protocol evaluating seven regions to determine brain concentrations of N-acetyl aspartate (NAA), creatine and phosphocreatine (Cr), cholines (Cho), myo-inositol, and a composite of glutamate and glutamine (GLX). Correlation and multiple linear regression analyses were conducted.

Results

Mean childhood blood lead levels were associated with regionally specific brain metabolite concentrations adjusted for age at imaging and Full-Scale intelligence quotient. Adjusted analyses estimated for a unit (micrograms per deciliter) increase in mean childhood blood lead concentrations, a decrease of NAA and Cr concentration levels in the basal ganglia, a decrease of NAA and a decrease of Cho concentration levels in the cerebellar hemisphere, a decrease of GLX concentration levels in vermis, a decrease of Cho and a decrease of GLX concentration levels in parietal white matter, and a decrease of Cho concentration levels in frontal white matter.

Conclusions

Gray-matter NAA reductions associated with increasing childhood blood lead levels suggest that sustained childhood lead exposure produces an irreversible pattern of neuronal dysfunction, whereas associated white-matter choline declines indicate a permanent alteration to myelin architecture.     

Exposure and Effect Assessment of Aerosolized Red Tide Toxins (Brevetoxins) and Asthma

Background

In previous studies we demonstrated statistically significant changes in reported symptoms for lifeguards, general beach goers, and persons with asthma, as well as statistically significant changes in pulmonary function tests (PFTs) in asthmatics, after exposure to brevetoxins in Florida red tide (Karenia brevis bloom) aerosols.

Objectives

In this study we explored the use of different methods of intensive ambient and personal air monitoring to characterize these exposures to predict self-reported health effects in our asthmatic study population.

Methods

We evaluated health effects in 87 subjects with asthma before and after 1 hr of exposure to Florida red tide aerosols and assessed for aerosolized brevetoxin exposure using personal and ambient samplers.

Results

After only 1 hr of exposure to Florida red tide aerosols containing brevetoxin concentrations > 57 ng/m³, asthmatics had statistically significant increases in self-reported respiratory symptoms and total symptom scores. However, we did not see the expected corresponding changes in PFT results. Significant increases in self-reported symptoms were also observed for those not using asthma medication and those living ≥ 1 mile from the coast.

Conclusions

These results provide additional evidence of health effects in asthmatics from ambient exposure to aerosols containing very low concentrations of brevetoxins, possibly at the lower threshold for inducing a biologic response (i.e., toxicity). Consistent with the literature describing self-reported symptoms as an accurate measure of asthmatic distress, our results suggest that self-reported symptoms are a valuable measure of the extent of health effects from exposure to aerosolized brevetoxins in asthmatic populations.     

Prenatal exposure to perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS) and maternally reported developmental milestones in infancy

Background

Perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) are fluorinated organic compounds present in the general population at low concentrations. Animal studies have shown that they may affect neuromuscular development at high concentrations.

Objectives

We investigated the association between plasma levels of PFOS and PFOA in pregnant women and motor and mental developmental milestones of their children.

Methods

We randomly selected 1,400 pairs of pregnant women and their children from the Danish National Birth Cohort. PFOS and PFOA were measured in maternal blood samples taken in early pregnancy. Apgar score was abstracted from the National Hospital Discharge Register in Denmark. Developmental milestones were reported by mothers using highly structured questionnaires when the children were around 6 months and 18 months of age.

Results

Mothers who had higher levels of PFOA and PFOS gave birth to children who had similar Apgar scores and reached virtually all of the development milestones at the same time as children born to mothers with lower exposure levels. Children who were born to mothers with higher PFOS levels were slightly more likely to start sitting without support at a later age.

Conclusion

We found no convincing associations between developmental milestones in early childhood and levels of PFOA or PFOS as measured in maternal plasma early in pregnancy.