Traffic-Related Particulate Matter and Acute Respiratory Symptoms among New York City Area Adolescents

Background

Exposure to traffic-related particulate matter (PM) has been associated with adverse respiratory health outcomes in children. Diesel exhaust particles (DEPs) are a local driver of urban fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)]; however, evidence linking ambient DEP exposure to acute respiratory symptoms is relatively sparse, and susceptibilities of urban and asthmatic children are inadequately characterized.

Objectives

We examined associations of daily ambient black carbon (BC) concentrations, a DEP indicator, with daily respiratory symptoms among asthmatic and nonasthmatic adolescents in New York City (NYC) and a nearby suburban community.

Methods

BC and PM_2.5 were monitored continuously outside three NYC high schools and one suburban high school for 4–6 weeks, and daily symptom data were obtained from 249 subjects (57 asthmatics, 192 nonasthmatics) using diaries. Associations between pollutants and symptoms were characterized using multilevel generalized linear mixed models, and modification by urban residence and asthma status were examined.

Results

Increases in BC were associated with increased wheeze, shortness of breath, and chest tightness. Multiple lags of nitrogen dioxide (NO₂) exposure were associated with symptoms. For several symptoms, associations with BC and NO₂ were significantly larger in magnitude among urban subjects and asthmatics compared with suburban subjects and nonasthmatics, respectively. PM_2.5 was not consistently associated with increases in symptoms.

Conclusions

Acute exposures to traffic-related pollutants such as DEPs and/or NO₂ may contribute to increased respiratory morbidity among adolescents, and urban residents and asthmatics may be at increased risk. The findings provide support for developing additional strategies to reduce diesel emissions further, especially in populations susceptible because of environment or underlying respiratory disease.     

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.     

The Costs of Respiratory Illnesses Arising from Florida Gulf Coast Karenia brevis Blooms

Background

Algal blooms of Karenia brevis, a harmful marine algae, occur almost annually off the west coast of Florida. At high concentrations, K. brevis blooms can cause harm through the release of potent toxins, known as brevetoxins, to the atmosphere. Epidemiologic studies suggest that aerosolized brevetoxins are linked to respiratory illnesses in humans.

Objectives

We hypothesized a relationship between K. brevis blooms and respiratory illness visits to hospital emergency departments (EDs) while controlling for environmental factors, disease, and tourism. We sought to use this relationship to estimate the costs of illness associated with aerosolized brevetoxins.

Methods

We developed a statistical exposure–response model to express hypotheses about the relationship between respiratory illnesses and bloom events. We estimated the model with data on ED visits, K. brevis cell densities, and measures of pollen, pollutants, respiratory disease, and intra-annual population changes.

Results

We found that lagged K. brevis cell counts, low air temperatures, influenza outbreaks, high pollen counts, and tourist visits helped explain the number of respiratory-specific ED diagnoses. The capitalized estimated marginal costs of illness for ED respiratory illnesses associated with K. brevis blooms in Sarasota County, Florida, alone ranged from $0.5 to $4 million, depending on bloom severity.

Conclusions

Blooms of K. brevis lead to significant economic impacts. The costs of illness of ED visits are a conservative estimate of the total economic impacts. It will become increasingly necessary to understand the scale of the economic losses associated with K. brevis blooms to make rational choices about appropriate mitigation.     

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.     

Self-Reported Truck Traffic on the Street of Residence and Symptoms of Asthma and Allergic Disease: A Global Relationship in ISAAC Phase 3

Background

Associations between traffic pollution on the street of residence and a range of respiratory and allergic outcomes in children have been reported in developed countries, but little is known about such associations in developing countries.

Methods

The third phase of the International Study of Asthma and Allergies in Childhood (ISAAC) was carried out in 13- to 14-year-old and 6- to 7-year-old children across the world. A question about frequency of truck traffic on the street of residence was included in an additional questionnaire. We investigated the association between self-reported truck traffic on the street of residence and symptoms of asthma, rhinoconjunctivitis, and eczema with logistic regression. Adjustments were made for sex, region of the world, language, gross national income, and 10 other subject-specific covariates.

Results

Frequency of truck traffic on the street of residence was positively associated with the prevalence of symptoms of asthma, rhinoconjunctivitis, and eczema with an exposure–response relationship. Odds ratios (95% confidence intervals) for “current wheeze” and “almost the whole day” versus “never” truck traffic were 1.35 (1.23–1.49) for 13- to 14-year-olds and 1.35 (1.22–1.48) for 6- to 7-year-olds.

Conclusions

Higher exposure to self-reported truck traffic on the street of residence is associated with increased reports of symptoms of asthma, rhinitis, and eczema in many locations in the world. These findings require further investigation in view of increasing exposure of the world’s children to traffic.     

Personal exposures to traffic-related air pollution and acute respiratory health among Bronx schoolchildren with asthma

Background

Previous studies have reported relationships between adverse respiratory health outcomes and residential proximity to traffic pollution, but have not shown this at a personal exposure level.

Objective

We compared, among inner-city children with asthma, the associations of adverse asthma outcome incidences with increased personal exposure to particulate matter mass ≤ 2.5 μm in aerodynamic diameter (PM_2.5) air pollution versus the diesel-related carbonaceous fraction of PM_2.5.

Methods

Daily 24-hr personal samples of PM_2.5, including the elemental carbon (EC) fraction, were collected for 40 fifth-grade children with asthma at four South Bronx schools (10 children per school) during approximately 1 month each. Spirometry and symptom scores were recorded several times daily during weekdays.

Results

We found elevated same-day relative risks of wheeze [1.45; 95% confidence interval (CI), 1.03–2.04)], shortness of breath (1.41; 95% CI, 1.01–1.99), and total symptoms (1.30; 95% CI, 1.04–1.62) with an increase in personal EC, but not with personal PM_2.5 mass. We found increased risk of cough, wheeze, and total symptoms with increased 1-day lag and 2-day average personal and school-site EC. We found no significant associations with school-site PM_2.5 mass or sulfur. The EC effect estimate was robust to addition of gaseous pollutants.

Conclusion

Adverse health associations were strongest with personal measures of EC exposure, suggesting that the diesel “soot” fraction of PM_2.5 is most responsible for pollution-related asthma exacerbations among children living near roadways. Studies that rely on exposure to PM mass may underestimate PM health impacts.     

Modifying effect of suicidal ideation on the relationship between asthma and cigarette use behaviors among Korean adolescents

Objectives

Although cigarette smoking is known to be related to the exacerbation of asthma symptoms, several studies have indicated that the prevalence of cigarette smoking among asthmatic adolescents is similar to or even higher than that among non-asthmatic adolescents. The aim of this study was to evaluate the relationship between asthma and cigarette use behaviors and whether or not the presence of suicidal ideation modifies this relationship among Korean adolescents.

Methods

We analyzed data from the 2008 Korea Youth Risk Behavior Web-based Survey, which included a nationally representative sample of middle and high school students. Multiple logistic regression models were used to calculate odd ratios and 95% confidence intervals of cigarette use behaviors among current asthmatics, former asthmatics, and non-asthmatics, after adjusting for gender, grade, school records, socioeconomic status, current alcohol use, and suicidal ideation.

Results

Of 75 238 study participants, 3.5% were current asthmatics and 4.5% were former asthmatics. Compared with non-asthmatics, asthmatics were more likely to report current cigarette use, frequent and heavy cigarette use, and cigarette use before 13 years of age. There were statistically significant interactions between asthma and suicidal ideation in cigarette use behaviors.

Conclusions

This study demonstrated that asthmatic adolescents are more likely than non-asthmatic adolescents to engage in cigarette use behaviors and the presence of suicidal ideation is an effect modifier of the relationship between asthma and cigarette use behaviors. Particular attention should be paid to the awareness of health risks of cigarette smoking and mental health problems among asthmatic adolescents.     

Symptoms and Medication Use in Children with Asthma and Traffic-Related Sources of Fine Particle Pollution

Background

Exposure to ambient fine particles [particulate matter ≤ 2.5 μm diameter (PM_2.5)] is a potential factor in the exacerbation of asthma. National air quality particle standards consider total mass, not composition or sources, and may not protect against health impacts related to specific components.

Objective

We examined associations between daily exposure to fine particle components and sources, and symptoms and medication use in children with asthma.

Methods

Children with asthma (n = 149) 4–12 years of age were enrolled in a year-long study. We analyzed particle samples for trace elements (X-ray fluorescence) and elemental carbon (light reflectance). Using factor analysis/source apportionment, we identified particle sources (e.g., motor vehicle emissions) and quantified daily contributions. Symptoms and medication use were recorded on study diaries. Repeated measures logistic regression models examined associations between health outcomes and particle exposures as elemental concentrations and source contributions.

Results

More than half of mean PM_2.5 was attributed to traffic-related sources motor vehicles (42%) and road dust (12%). Increased likelihood of symptoms and inhaler use was largest for 3-day averaged exposures to traffic-related sources or their elemental constituents and ranged from a 10% increased likelihood of wheeze for each 5-μg/m³ increase in particles from motor vehicles to a 28% increased likelihood of shortness of breath for increases in road dust. Neither the other sources identified nor PM_2.5 alone was associated with increased health outcome risks.

Conclusions

Linking respiratory health effects to specific particle pollution composition or sources is critical to efforts to protect public health. We associated increased risk of symptoms and inhaler use in children with asthma with exposure to traffic-related fine particles.     

Do TETRA (Airwave) Base Station Signals Have a Short-Term Impact on Health and Well-Being? A Randomized Double-Blind Provocation Study

Background

“Airwave” is the new communication system currently being rolled out across the United Kingdom for the police and emergency services, based on the Terrestrial Trunked Radio Telecommunications System (TETRA). Some police officers have complained about skin rashes, nausea, headaches, and depression as a consequence of using their Airwave handsets. In addition, a small subgroup in the population self-report being sensitive to electromagnetic fields (EMFs) in general.

Objectives

We conducted a randomized double-blind provocation study to establish whether short-term exposure to a TETRA base station signal has an impact on the health and well-being of individuals with self-reported “electrosensitivity” and of participants who served as controls.

Methods

Fifty-one individuals with self-reported electrosensitivity and 132 age- and sex-matched controls participated in an open provocation test; 48 sensitive and 132 control participants went on to complete double-blind tests in a fully screened semianechoic chamber. Heart rate, skin conductance, and blood pressure readings provided objective indices of short-term physiological response. Visual analog scales and symptom scales provided subjective indices of well-being.

Results

We found no differences on any measure between TETRA and sham (no signal) under double-blind conditions for either controls or electrosensitive participants, and neither group could detect the presence of a TETRA signal at rates greater than chance (50%). When conditions were not double blind, however, the self-reported electrosensitive individuals did report feeling worse and experienced more severe symptoms during TETRA compared with sham.

Conclusions

Our findings suggest that the adverse symptoms experienced by electrosensitive individuals are due to the belief of harm from TETRA base stations rather than to the low-level EMF exposure itself.     

Short-Term Effects of Air Pollution on Wheeze in Asthmatic Children in Fresno,California

Background

Although studies have demonstrated that air pollution is associated with exacerbation of asthma symptoms in children with asthma, little is known about the susceptibility of subgroups, particularly those with atopy.

Objective

This study was designed to evaluate our a priori hypothesis that identifiable subgroups of asthmatic children are more likely to wheeze with exposure to ambient air pollution.

Methods

A cohort of 315 children with asthma, 6–11 years of age, was recruited for longitudinal follow-up in Fresno, California (USA). During the baseline visit, children were administered a respiratory symptom questionnaire and allergen skin-prick test. Three times a year, participants completed 14-day panels during which they answered symptom questions twice daily. Ambient air quality data from a central monitoring station were used to assign exposures to the following pollutants: particulate matter ≤ 2.5 μm in aerodynamic diameter, particulate matter between 2.5 and 10 μm in aerodynamic diameter (PM_10–2.5), elemental carbon, nitrogen dioxide (NO₂), nitrate, and O₃.

Results

For the group as a whole, wheeze was significantly associated with short-term exposures to NO₂ [odds ratio (OR) = 1.10 for 8.7-ppb increase; 95% confidence interval (CI), 1.02–1.20] and PM_10–2.5 (OR = 1.11 for 14.7-μg/m³ increase; 95% CI, 1.01–1.22). The association with wheeze was stronger for these two pollutants in children who were skin-test positive to cat or common fungi and in boys with mild intermittent asthma.

Conclusion

A pollutant associated with traffic emissions, NO₂, and a pollutant with bioactive constituents, PM_10–2.5, were associated with increased risk of wheeze in asthmatic children living in Fresno, California. Children with atopy to cat or common fungi and boys with mild intermittent asthma were the subgroups for which we observed the largest associations.     

Respiratory and other health effects reported in children exposed to the World Trade Center disaster of 11 September 2001

Background

Effects of the World Trade Center (WTC) disaster on children’s respiratory health have not been definitively established.

Objective

This report describes respiratory health findings among children who were < 18 years of age on 11 September 2001 (9/11) and examine associations between disaster-related exposures and respiratory health.

Methods

Children recruited for the WTC Health Registry (WTCHR) included child residents and students (kindergarten through 12th grade) in Manhattan south of Canal Street, children who were south of Chambers Street on 9/11, and adolescent disaster-related workers or volunteers. We collected data via computer-assisted telephone interviews in 2003–2004, with interview by adult proxy for children still < 18 years of age at that time. We compared age-specific asthma prevalence with National Health Interview Survey estimates.

Results

Among 3,184 children enrolled, 28% were < 5 years of age on 9/11; 34%, 5–11 years; and 39%, 12–17 years. Forty-five percent had a report of dust cloud exposure on 9/11. Half (53%) reported at least one new or worsened respiratory symptom, and 5.7% reported new asthma diagnoses. Before 9/11, age-specific asthma prevalence in enrolled children was similar to national estimates, but prevalence at interview was elevated among enrollees < 5 years of age. Dust cloud exposure was associated with new asthma diagnosis (adjusted odds ratio = 2.3; 95% confidence interval, 1.5–3.5).

Conclusions

Asthma prevalence after 9/11 among WTCHR enrollees < 5 years of age was higher than national estimates, and new asthma diagnosis was associated with dust cloud exposure in all age groups. We will determine severity of asthma and persistence of other respiratory symptoms on follow-up surveys.     

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.     

A longitudinal study of indoor nitrogen dioxide levels and respiratory symptoms in inner-city children with asthma

Background

The effect of indoor nitrogen dioxide concentrations on asthma morbidity among inner-city preschool children is uncertain.

Objectives

Our goal was to estimate the effect of indoor NO₂ concentrations on asthma morbidity in an inner-city population while adjusting for other indoor pollutants.

Methods

We recruited 150 children (2–6 years of age) with physician-diagnosed asthma from inner-city Baltimore, Maryland. Indoor air was monitored over a 72-hr period in the children’s bedrooms at baseline and 3 and 6 months. At each visit, the child’s caregiver completed a questionnaire assessing asthma symptoms over the previous 2 weeks and recent health care utilization.

Results

Children were 58% male, 91% African American, and 42% from households with annual income < $25,000; 63% had persistent asthma symptoms. The mean (± SD) in-home NO₂ concentration was 30.0 ± 33.7 (range, 2.9–394.0) ppb. The presence of a gas stove and the use of a space heater or oven/stove for heat were independently associated with higher NO₂ concentrations. Each 20-ppb increase in NO₂ exposure was associated significantly with an increase in the number of days with limited speech [incidence rate ratio (IRR) = 1.15; 95% confidence interval (CI), 1.05–1.25], cough (IRR = 1.10; 95% CI, 1.02–1.18), and nocturnal symptoms (IRR = 1.09; 95% CI, 1.02–1.16), after adjustment for potential confounders. NO₂ concentrations were not associated with increased health care utilization.

Conclusions

Higher indoor NO₂ concentrations were associated with increased asthma symptoms in preschool inner-city children. Interventions aimed at lowering NO₂ concentrations in inner-city homes may reduce asthma morbidity in this vulnerable population.     

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.     

Electrocardiographic ST-segment depression and exposure to traffic-related aerosols in elderly subjects with coronary artery disease

Background

Air pollutants have not been associated with ambulatory electrocardiographic evidence of ST-segment depression ≥ 1 mm (probable cardiac ischemia). We previously found that markers of primary (combustion-related) organic aerosols and gases were positively associated with circulating biomarkers of inflammation and ambulatory blood pressure in the present cohort panel study of elderly subjects with coronary artery disease.

Objectives

We specifically aimed to evaluate whether exposure markers of primary organic aerosols and ultrafine particles were more strongly associated with ST-segment depression of ≥ 1 mm than were secondary organic aerosols or PM_2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) mass.

Methods

We evaluated relations of air pollutants to ambulatory electrocardiographic evidence of cardiac ischemia over 10 days in 38 subjects without ST depression on baseline electrocardiographs. Exposures were measured outdoors in retirement communities in the Los Angeles basin, including daily size-fractionated particle mass and hourly markers of primary and secondary organic aerosols and gases. Generalized estimating equations were used to estimate odds of hourly ST-segment depression (≥ 1 mm) from hourly air pollution exposures and to estimate relative rates of daily counts of ST-segment depression from daily average exposures, controlling for potential confounders.

Results

We found significant positive associations of hourly ST-segment depression with markers of combustion-related aerosols and gases averaged 1-hr through 3–4 days, but not secondary (photochemically aged) organic aerosols or ozone. The odds ratio per interquartile increase in 2-day average primary organic carbon (5.2 μg/m³) was 15.4 (95% confidence interval, 3.5–68.2). Daily counts of ST-segment depression were consistently associated with primary combustion markers and 2-day average quasi-ultrafine particles < 0.25 μm.

Conclusions

Results suggest that exposure to quasi-ultrafine particles and combustion-related pollutants (predominantly from traffic) increase the risk of myocardial ischemia, coherent with our previous findings for systemic inflammation and blood pressure.     

Childhood Asthma and Environmental Exposures at Swimming Pools: State of the Science and Research Recommendations

Objectives

Recent studies have explored the potential for swimming pool disinfection by-products (DBPs), which are respiratory irritants, to cause asthma in young children. Here we describe the state of the science on methods for understanding children’s exposure to DBPs and biologics at swimming pools and associations with new-onset childhood asthma and recommend a research agenda to improve our understanding of this issue.

Data sources

A workshop was held in Leuven, Belgium, 21–23 August 2007, to evaluate the literature and to develop a research agenda to better understand children’s exposures in the swimming pool environment and their potential associations with new-onset asthma. Participants, including clinicians, epidemiologists, exposure scientists, pool operations experts, and chemists, reviewed the literature, prepared background summaries, and held extensive discussions on the relevant published studies, knowledge of asthma characterization and exposures at swimming pools, and epidemiologic study designs.

Synthesis

Childhood swimming and new-onset childhood asthma have clear implications for public health. If attendance at indoor pools increases risk of childhood asthma, then concerns are warranted and action is necessary. If there is no such relationship, these concerns could unnecessarily deter children from indoor swimming and/or compromise water disinfection.

Conclusions

Current evidence of an association between childhood swimming and new-onset asthma is suggestive but not conclusive. Important data gaps need to be filled, particularly in exposure assessment and characterization of asthma in the very young. Participants recommended that additional evaluations using a multidisciplinary approach are needed to determine whether a clear association exists.     

Pesticide Exposure and Hypertensive Disorders During Pregnancy

Background

Hypertensive disorders of pregnancy, including pregnancy-induced hypertension (PIH) and preeclampsia (PE), complicate 2–8% of pregnancies. Few studies have examined environmental risk factors in relation to these conditions.

Objectives

Our goal was to examine whether pesticide exposure during pregnancy was associated with hypertensive disorders of pregnancy.

Methods

We analyzed self-reported data from 11,274 wives of farmers enrolled in the Agricultural Health Study (AHS) between 1993 and 1997. Using logistic regression models, we estimated the adjusted odds ratios (AORs) for PIH and PE associated with pesticide-related activities during the first trimester of pregnancy.

Results

First-trimester residential and agricultural activities with potential exposure to pesticides were associated with both PIH [residential AOR = 1.27; 95% confidence interval (CI), 1.02–1.60; agricultural AOR = 1.60; 95% CI, 1.05–2.45] and PE (residential AOR = 1.32; 95% CI, 1.02–1.70; agricultural AOR = 2.07; 95% CI, 1.34–3.21).

Conclusions

Exposure to pesticides during pregnancy may increase the risk of hypertensive disorders of pregnancy. Laboratory research may provide insights into relationships between pesticide exposure and hypertensive diseases of pregnancy.     

Acute decreases in proteasome pathway activity after inhalation of fresh diesel exhaust or secondary organic aerosol

Background

Epidemiologic studies consistently demonstrate an association between acute cardiopulmonary events and changes in air pollution; however, the mechanisms that underlie these associations are not completely understood. Oxidative stress and inflammation have been suggested to play a role in human responses to air pollution. The proteasome is an intracellular protein degradation system linked to both of these processes and may help mediate air pollution effects.

Objectives

In these studies, we determined whether acute experimental exposure to two different aerosols altered white blood cell (WBC) or red blood cell (RBC) proteasome activity in human subjects. One aerosol was fresh diesel exhaust (DE), and the other freshly generated secondary organic aerosol (SOA).

Methods

Thirty-eight healthy subjects underwent 2-hr resting inhalation exposures to DE and separate exposures to clean air (CA); 26 subjects were exposed to DE, CA, and SOA. CA responses were subtracted from DE or SOA responses, and mixed linear models with F-tests were used to test the effect of exposure to each aerosol on WBC and RBC proteasome activity.

Results

WBC proteasome activity was reduced 8% (p = 0.04) after exposure to either DE or SOA and decreased by 11.5% (p = 0.03) when SOA was analyzed alone. RBCs showed similar 8–10% declines in proteasome activity (p = 0.05 for DE alone).

Conclusions

Air pollution produces oxidative stress and inflammation in many experimental models, including humans. Two experimental aerosols caused rapid declines in proteasome activity in peripheral blood cells, supporting a key role for the proteasome in acute human responses to air pollution.     

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.     

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.