Real-world cell phone radiofrequency electromagnetic field exposures.

In 2011 the International Agency for Research on Cancer classified radiofrequency electromagnetic fields (RF EMF) from cell phones as possibly carcinogenic to humans. The National Toxicology Program and the Ramazzini Institute have both reported that RF EMF exposures significantly increase gliomas and Schwannomas of the heart in rodent studies. Recent studies indicate that RF EMF exposures from cell phones have negative impacts on animal cells and cognitive and/or behavioral development in children. Case-control epidemiological studies have found evidence for cell phone use and increased risk for glioma and localization of the glioma associated with the consistent exposure site of regular cell phone use. Understanding the exposure level, or power density, from RF EMF emitted by cell phones under real-world usage and signal reception conditions, as distinct from the published measurements of maximum Specific Absorption Rate values, may help cell phone users decide whether to take behavioral steps to reduce RF EMF exposure. Exposure measurements were conducted on phone models from four major mobile network operators (MNOs) in the USA for calls received under strong and weak reception signal conditions, near the phone face and at several distances up to 48 cm. RF EMF exposure from all phones was found to be greater under weak (1-2 display bars) than under strong (4-5 display bars) reception signal conditions by up to four orders of magnitude. Notably, RF EMF exposure levels under weak reception signal conditions at a distance of 48 cm from the phone were similar to or greater than those detected under strong reception signal conditions at a distance of 4 cm. Under weak reception signal conditions, power density reductions of up to 90% occurred at 16 cm typical for speaker phone or texting over the 4 cm near-ear exposure. The results of this investigation of second-generation (2G) technology suggest that reduced and precautionary use of cell phones under weak signal conditions could lower a user's RF EMF exposure by up to several orders of magnitude. Bluetooth headset power density exposures were 10-400 times lower than those of the cell phones to which they were connected and dependent on the headset rather than the connected phone. The results of this study informed the development of public health guidance regarding cell phone use.

Evaluation of the accuracy of a UWB tracker for in-home positioning for older adults.

The population of older adults is rapidly growing. In-home monitoring systems have been used to support aging-in-place. Ambient sensors or wearable localizers can be used but may be too low resolution, while camera systems are invasive to privacy. Ultra-wideband (UWB) localization offers precise positioning by placing anchors throughout the house and wearing a tag that is tracked by the anchors. In this study, the accuracy of UWB for indoor tracking was evaluated in a motion capture gait lab and in a mock condo in the Glenrose Rehabilitation Hospital. First, the configuration of UWB was tested, changing factors related to sampling time, anchor placement and line-of-sight. Comparing these factors to the configurations recommended by the manufacturer guidelines, accuracies remained within 14 cm. We then performed static and dynamic accuracy tests, with dynamic testing comprised of rolling and walking motions. In the motion capture lab, we found localization accuracies of 7.0 ± 11.1 cm while in the mock condo, we found accuracies of 27.3 ± 12.9 cm. Dynamic testing with rolling motions had an average of 19.1 ± 1.6 cm while walking was 20.5 ± 4.2 cm. The mean accuracy of UWB is within the 30 cm target for indoor localization.

Long-term exposure to air pollution and cardiorespiratory disease in the California teachers study cohort.

RATIONALE: Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease. OBJECTIVES: To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction and stroke, as well as all-cause and cause specific mortality. METHODS: We estimated long-term residential air pollution exposure for more than 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals.We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident myocardial infarction and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models. MEASUREMENTS AND MAIN RESULTS: We found elevated hazard ratios linking long-term exposure to particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5), scaled to an increment of 10 µg/m3 with mortality from ischemic heart disease (IHD) (1.20; 95% confidence interval [CI], 1.02-1.41) and, particularly among postmenopausal women, incident stroke (1.19; 95% CI, 1.02-1.38). Long-term exposure to particulate matter less than 10 µm in aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06; 95% CI, 0.99-1.14) and incident stroke (1.06; 95% CI, 1.00-1.13), while exposure to nitrogen oxides was associated with elevated risks for IHD and all cardiovascular mortality. CONCLUSIONS: This study provides evidence linking long-term exposure to PM2.5 and PM10 with increased risks of incident stroke as well as IHD mortality; exposure to nitrogen oxides was also related to death from cardiovascular diseases.

Exposure to air pollution in critical prenatal time windows and IgE levels in newborns.

The objective of this study was to analyze the mechanisms by which exposure to ambient air pollutants influences respiratory health may include altered prenatal immune development. To analyze associations between elevated cord serum Immunoglobulin E (IgE) levels and maternal air pollution exposure during each month of gestation. Total cord serum IgE was determined by the CAP system and mothers' total IgE levels by nephelometry for 459 births in the Czech Republic from May 1994 to mid-January 1997. Concentrations of polycyclic aromatic hydrocarbons (PAHs) and particulate matter <2.5 microns in diameter (PM(2.5) ) were measured in ambient air, and arithmetic means were calculated for each gestational month. Log binomial regression models were used to estimate prevalence ratios (PR) for elevated cord serum IgE (≥0.9 IU/ml) adjusting for district of residence, year of birth, and in further models, for maternal IgE (a surrogate for atopy) and gestational season. Heterogeneity by maternal atopy status was evaluated for associations of air pollution and of cigarette smoke. In adjusted models, PAH and PM(2.5) exposures in the second month of gestation were each associated with a lower prevalence of elevated cord serum IgE. For an average increase of 100 ng/m(3) of PAHs, the PR was 0.69 (95% confidence interval (CI): 0.50, 0.95); for 25 µg/m(3) increase in PM(2.5) , the PR was 0.77 (95% CI: 0.55, 1.07). Conversely, exposures later in gestation were associated with a higher prevalence of elevated cord IgE: in the fifth month, the PR for PAH exposure was 1.64 (95% CI: 1.29, 2.08), while for PM(2.5) in the sixth month, it was 1.66 (95% CI: 1.30, 2.13). In analyses stratified by maternal atopy, air pollutants were associated with altered cord serum IgE only among neonates with non-atopic mothers. Similarly, an association of cigarette smoke with elevated cord serum IgE was found only in non-atopic mothers. PAHs and PM(2.5) , constituents of both ambient air pollution and cigarette smoke, appear to influence fetal immune development, particularly among infants whose mothers are not atopic.

Air pollution exposure during critical time periods in gestation and alterations in cord blood lymphocyte distribution: a cohort of livebirths.

BACKGROUND: Toxic exposures have been shown to influence maturation of the immune system during gestation. This study investigates the association between cord blood lymphocyte proportions and maternal exposure to air pollution during each gestational month. METHODS: Cord blood was analyzed using a FACSort flow cytometer to determine proportions of T lymphocytes (CD3+ cells and their subsets, CD4+ and CD8+), B lymphocytes (CD19+) and natural killer (NK) cells. Ambient air concentrations of 12 polycyclic aromatic hydrocarbons (PAH) and particulate matter < 2.5 micrometer in diameter (PM2.5) were measured using fixed site monitors. Arithmetic means of these pollutants, calculated for each gestational month, were used as exposure metrics. Data on covariates were obtained from medical records and questionnaires. Multivariable linear regression models were fitted to estimate associations between monthly PAH or PM2.5 and cord blood lymphocytes, adjusting for year of birth and district of residence and, in further models, gestational season and number of prior live births. RESULTS: The adjusted models show significant associations between PAHs or PM2.5 during early gestation and increases in CD3+ and CD4+ lymphocytes percentages and decreases in CD19+ and NK cell percentages in cord blood. In contrast, exposures during late gestation were associated with decreases in CD3+ and CD4+ fractions and increases in CD19+ and NK cell fractions. There was no significant association between alterations in lymphocyte distribution and air pollution exposure during the mid gestation. CONCLUSIONS: PAHs and PM2.5 in ambient air may influence fetal immune development via shifts in cord blood lymphocytes distributions. Associations appear to differ by exposure in early versus late gestation.

Residential traffic and children's respiratory health.

BACKGROUND: Living near traffic has been associated with asthma and other respiratory symptoms. Most studies, however, have been conducted in areas with high background levels of ambient air pollution, making it challenging to isolate an independent effect of traffic. Additionally, most investigations have used surrogates of exposure, and few have measured traffic pollutants directly as part of the study. OBJECTIVE: We conducted a cross-sectional study of current asthma and other respiratory symptoms in children (n = 1,080) living at varying distances from high-traffic roads in the San Francisco Bay Area, California, a highly urbanized region characterized by good regional air quality due to coastal breezes. METHODS: We obtained health information and home environmental factors by parental questionnaire. We assessed exposure with several measures of residential proximity to traffic calculated using geographic information systems, including traffic within a given radius and distance to major roads. We also measured traffic-related pollutants (nitrogen oxides and nitrogen dioxide) for a subset of households to determine how well traffic metrics correlated with measured traffic pollutants. RESULTS: Using multivariate logistic regression analyses, we found associations between current asthma and residential proximity to traffic. For several traffic metrics, children whose residences were in the highest quintile of exposure had approximately twice the adjusted odds of current asthma (i.e., asthma episode in the preceeding 12 months) compared with children whose residences were within the lowest quintile. The highest risks were among those living within 75 m of a freeway/highway. Most traffic metrics correlated moderately well with actual pollutant measurements. CONCLUSION: Our findings provide evidence that even in an area with good regional air quality, proximity to traffic is associated with adverse respiratory health effects in children.

The effects of components of fine particulate air pollution on mortality in california: results from CALFINE.

OBJECTIVE: Several epidemiologic studies provide evidence of an association between daily mortality and particulate matter < 2.5 pm in diameter (PM2.5). Little is known, however, about the relative effects of PM2.5 constituents. We examined associations between 19 PM2.5 components and daily mortality in six California counties. DESIGN: We obtained daily data from 2000 to 2003 on mortality and PM2.5 mass and components, including elemental and organic carbon (EC and OC), nitrates, sulfates, and various metals. We examined associations of PM2.5 and its constituents with daily counts of several mortality categories: all-cause, cardiovascular, respiratory, and mortality age > 65 years. Poisson regressions incorporating natural splines were used to control for time-varying covariates. Effect estimates were determined for each component in each county and then combined using a random-effects model. RESULTS: PM2.5 mass and several constituents were associated with multiple mortality categories, especially cardiovascular deaths. For example, for a 3-day lag, the latter increased by 1.6, 2.1, 1.6, and 1.5% for PM2.5, EC, OC, and nitrates based on interquartile ranges of 14.6, 0.8, 4.6, and 5.5 pg/m(3), respectively. Stronger associations were observed between mortality and additional pollutants, including sulfates and several metals, during the cool season. CONCLUSION: This multicounty analysis adds to the growing body of evidence linking PM2.5 with mortality and indicates that excess risks may vary among specific PM2.5 components. Therefore, the use of regression coefficients based on PM2.5 mass may underestimate associations with some PM2.5 components. Also, our findings support the hypothesis that combustion-associated pollutants are particularly important in California.

Early childhood lower respiratory illness and air pollution.

BACKGROUND: Few studies of air pollutants address morbidity in preschool children. In this study we evaluated bronchitis in children from two Czech districts: Teplice, with high ambient air pollution, and Prachatice, characterized by lower exposures. OBJECTIVES: Our goal was to examine rates of lower respiratory illnesses in preschool children in relation to ambient particles and hydrocarbons. METHODS: Air monitoring for particulate matter < 2.5 microm in diameter (PM(2.5)) and polycyclic aromatic hydrocarbons (PAHs) was conducted daily, every third day, or every sixth day. Children born May 1994 through December 1998 were followed to 3 or 4.5 years of age to ascertain illness diagnoses. Mothers completed questionnaires at birth and at follow-up regarding demographic, lifestyle, reproductive, and home environmental factors. Longitudinal multivariate repeated-measures analysis was used to quantify rate ratios for bronchitis and for total lower respiratory illnesses in 1,133 children. RESULTS: After adjustment for season, temperature, and other covariates, bronchitis rates increased with rising pollutant concentrations. Below 2 years of age, increments in 30-day averages of 100 ng/m(3) PAHs and of 25 microg/m(3) PM(2.5) resulted in rate ratios (RRs) for bronchitis of 1.29 [95 % confidence interval (CI), 1.07-1.54] and 1.30 (95% CI, 1.08-1.58), respectively; from 2 to 4.5 years of age, these RRs were 1.56 (95% CI, 1.22-2.00) and 1.23 (95% CI, 0.94-1.62), respectively. CONCLUSION: Ambient PAHs and fine particles were associated with early-life susceptibility to bronchitis. Associations were stronger for longer pollutant-averaging periods and, among children > 2 years of age, for PAHs compared with fine particles. Preschool-age children may be particularly vulnerable to air pollution-induced illnesses.

An association between asthma and BMI in adolescents: results from the California Healthy Kids Survey.

We examined the relationship between asthma prevalence and BMI in a cross-sectional survey of 471,969 adolescents. The size of the survey allowed us to investigate this relationship with much greater resolution than previously possible. Both lifetime and current asthma prevalence increased monotonically with increasing BMI, starting with individuals as low as the 45th to 55th percentiles of BMI. The pattern was similar between males and females and among six racial/ethnic groups. The results suggest that weight reduction even among persons not classified as overweight or obese may be an important component of asthma management.

Woodsmoke health effects: a review.

The sentiment that woodsmoke, being a natural substance, must be benign to humans is still sometimes heard. It is now well established, however, that wood-burning stoves and fireplaces as well as wildland and agricultural fires emit significant quantities of known health-damaging pollutants, including several carcinogenic compounds. Two of the principal gaseous pollutants in woodsmoke, CO and NOx, add to the atmospheric levels of these regulated gases emitted by other combustion sources. Health impacts of exposures to these gases and some of the other woodsmoke constituents (e.g., benzene) are well characterized in thousands of publications. As these gases are indistinguishable no matter where they come from, there is no urgent need to examine their particular health implications in woodsmoke. With this as the backdrop, this review approaches the issue of why woodsmoke may be a special case requiring separate health evaluation through two questions. The first question we address is whether woodsmoke should be regulated and/or managed separately, even though some of its separate constituents are already regulated in many jurisdictions. The second question we address is whether woodsmoke particles pose different levels of risk than other ambient particles of similar size. To address these two key questions, we examine several topics: the chemical and physical nature of woodsmoke; the exposures and epidemiology of smoke from wildland fires and agricultural burning, and related controlled human laboratory exposures to biomass smoke; the epidemiology of outdoor and indoor woodsmoke exposures from residential woodburning in developed countries; and the toxicology of woodsmoke, based on animal exposures and laboratory tests. In addition, a short summary of the exposures and health effects of biomass smoke in developing countries is provided as an additional line of evidence. In the concluding section, we return to the two key issues above to summarize (1) what is currently known about the health effects of inhaled woodsmoke at exposure levels experienced in developed countries, and (2) whether there exists sufficient reason to believe that woodsmoke particles are sufficiently different to warrant separate treatment from other regulated particles. In addition, we provide recommendations for additional woodsmoke research.

Fine particulate air pollution and mortality in nine California counties: results from CALFINE.

Many epidemiologic studies provide evidence of an association between daily counts of mortality and ambient particulate matter<10 microm in diameter (PM10). Relatively few studies, however, have investigated the relationship of mortality with fine particles [PM<2.5 microm in diameter (PM2.5)], especially in a multicity setting. We examined associations between PM2.5 and daily mortality in nine heavily populated California counties using data from 1999 through 2002. We considered daily counts of all-cause mortality and several cause-specific subcategories (respiratory, cardiovascular, ischemic heart disease, and diabetes). We also examined these associations among several subpopulations, including the elderly (>65 years of age), males, females, non-high school graduates, whites, and Hispanics. We used Poisson multiple regression models incorporating natural or penalized splines to control for covariates that could affect daily counts of mortality, including time, seasonality, temperature, humidity, and day of the week. We used meta-analyses using random-effects models to pool the observations in all nine counties. The analysis revealed associations of PM2.5 levels with several mortality categories. Specifically, a 10-microg/m3 change in 2-day average PM2.5 concentration corresponded to a 0.6% (95% confidence interval, 0.2-1.0%) increase in all-cause mortality, with similar or greater effect estimates for several other subpopulations and mortality subcategories, including respiratory disease, cardiovascular disease, diabetes, age>65 years, females, deaths out of the hospital, and non-high school graduates. Results were generally insensitive to model specification and the type of spline model used. This analysis adds to the growing body of evidence linking PM2.5 with daily mortality.

Early environmental exposures and intracellular Th1/Th2 cytokine profiles in 24-month-old children living in an agricultural area.

BACKGROUND: Children who reside in agricultural settings are potentially exposed to higher levels of organophosphate (OP) pesticides, endotoxin, and allergens than their urban counterparts. Endotoxin and allergens stimulate maturation of the immune response in early childhood, but little is known about the effect of exposures to OPs or to the three combined. OBJECTIVES: In this study, we investigated the relationships between these exposures and T-helper 1 (Th1) and T-helper 2 (Th2) cytokines, biomarkers of allergic asthma, in the subjects of CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas), a longitudinal birth cohort in Salinas Valley, California. Exposures were ascertained by interviewer-administered questionnaires and by home visits, and clinical diagnoses were abstracted from medical records. Blood samples were collected at 12 and 24 months of age and analyzed for Th1/Th2 status by flow cytometric detection of intracellular interferon-gamma/interleukin-4 cytokine expression. FINDINGS: Mean Th2 levels were significantly higher in children with doctor-diagnosed asthma and children with wheezing at 2 years of age. In a multiple linear regression model, exclusive breast-feeding at 1 month and pet ownership were associated with 35.3% (p < 0.01) and 34.5% (p = 0.01) increases in Th1, respectively. Maternal agricultural work and presence of gas stove in the home were associated with a 25.9% increase (p = 0.04) and 46.5% increase (p < 0.01) in Th2, respectively. CONCLUSIONS: Asthma and wheeze outcomes in children at 24 months of age are associated with elevated Th2 status in children at an early age. Our data further suggest that early exposures to an agricultural environment, breast-feeding, pets, and gas stoves affect the development of children's Th1/Th2 immune response.

Coarse particles and heart rate variability among older adults with coronary artery disease in the Coachella Valley, California.

Alterations in cardiac autonomic control, assessed by changes in heart rate variability (HRV), provide one plausible mechanistic explanation for consistent associations between exposure to airborne particulate matter (PM) and increased risks of cardiovascular mortality. Decreased HRV has been linked with exposures to PM10 (PM with aerodynamic diameter

Air pollution and cardiovascular disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association.

Air pollution is a heterogeneous, complex mixture of gases, liquids, and particulate matter. Epidemiological studies have demonstrated a consistent increased risk for cardiovascular events in relation to both short- and long-term exposure to present-day concentrations of ambient particulate matter. Several plausible mechanistic pathways have been described, including enhanced coagulation/thrombosis, a propensity for arrhythmias, acute arterial vasoconstriction, systemic inflammatory responses, and the chronic promotion of atherosclerosis. The purpose of this statement is to provide healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease. In addition, the implications of these findings in relation to public health and regulatory policies are addressed. Practical recommendations for healthcare providers and their patients are outlined. In the final section, suggestions for future research are made to address a number of remaining scientific questions.

Lessons Learned for the Study of Childhood Asthma from the Centers for Children's Environmental Health and Disease Prevention Research.

The National Children's Study will address, among other illnesses, the environmental causes of both incident asthma and exacerbations of asthma in children. Seven of the Centers for Children's Environmental Health and Disease Prevention Research (Children's Centers), funded by the National Institute of Environmental Health Sciences and the U.S. Environmental Protection Agency, conducted studies relating to asthma. The design of these studies was diverse and included cohorts, longitudinal studies of older children, and intervention trials involving asthmatic children. In addition to the general lessons provided regarding the conduct of clinical studies in both urban and rural populations, these studies provide important lessons regarding the successful conduct of community research addressing asthma. They demonstrate that it is necessary and feasible to conduct repeated evaluation of environmental exposures in the home to address environmental exposures relevant to asthma. The time and staff required were usually underestimated by the investigators, but through resourceful efforts, the studies were completed with a remarkably high completion rate. The definition of asthma and assessment of disease severity proved to be complex and required a combination of questionnaires, pulmonary function tests, and biologic samples for markers of immune response and disease activity. The definition of asthma was particularly problematic in younger children, who may exhibit typical asthma symptoms sporadically with respiratory infections without developing chronic asthma. Medications confounded the definition of asthma disease activity, and must be repeatedly and systematically estimated. Despite these many challenges, the Children's Centers successfully conducted long-term studies of asthma.

Association of housing disrepair indicators with cockroach and rodent infestations in a cohort of pregnant Latina women and their children.

Health burdens associated with poor housing and indoor pest infestations are likely to affect young children in particular, who spend most of their time indoors at home. We completed environmental assessments in 644 homes of pregnant Latina women and their children living in the Salinas Valley, California. High residential densities were common, with 39% of homes housing > 1.5 persons per room. Housing disrepair was also common: 58% of homes had peeling paint, 43% had mold, 25% had water damage, and 11% had rotting wood. Evidence of cockroaches and rodents was present in 60% and 32% of homes, respectively. Compared with representative national survey data from the U.S. Department of Housing and Urban Development, homes in our sample were more likely to have rodents, peeling paint, leaks under sinks, and much higher residential densities. The odds of rodent infestations in homes increased in the presence of peeling paint [odds ratio (OR) 2.1; 95% confidence interval (CI), 1.5-3.1], water damage (OR 1.9; 95% CI, 1.2-2.7), and mold (OR 1.5; 95% CI, 1.0-2.1). The odds of cockroach infestation increased in the presence of peeling paint (OR 3.8; 95% CI, 2.7-5.6), water damage (OR 1.9; 95% CI, 1.2-2.9), or high residential density (OR 2.1; 95% CI, 1.2-3.8). Homes that were less clean than average were more prone to both types of infestations. Pesticides were stored or used in 51% of households, partly to control roach and rodent infestations. These data indicate that adverse housing conditions are common in this community and increase the likelihood of pest infestations and home pesticide use. Interventions to improve housing and promote children's health and safety in this population are needed.

Air pollution and lymphocyte phenotype proportions in cord blood.

Effects of air pollution on morbidity and mortality may be mediated by alterations in immune competence. In this study we examined short-term associations of air pollution exposures with lymphocyte immunophenotypes in cord blood among 1,397 deliveries in two districts of the Czech Republic. We measured fine particulate matter < 2.5 microm in diameter (PM2.5) and 12 polycyclic aromatic hydrocarbons (PAHs) in 24-hr samples collected by versatile air pollution samplers. Cord blood samples were analyzed using a FACSort flow cytometer to determine phenotypes of CD3+ T-lymphocytes and their subsets CD4+ and CD8+, CD19+ B-lymphocytes, and natural killer cells. The mothers were interviewed regarding sociodemographic and lifestyle factors, and medical records were abstracted for obstetric, labor and delivery characteristics. During the period 1994 to 1998, the mean daily ambient concentration of PM2.5 was 24.8 microg/m3 and that of PAHs was 63.5 ng/m3. In multiple linear regression models adjusted for temperature, season, and other covariates, average PAH or PM2.5 levels during the 14 days before birth were associated with decreases in T-lymphocyte phenotype fractions (i.e., CD3+ CD4+, and CD8+), and a clear increase in the B-lymphocyte (CD19+) fraction. For a 100-ng/m3 increase in PAHs, which represented approximately two standard deviations, the percentage decrease was -3.3% [95% confidence interval (CI), -5.6 to -1.0%] for CD3+, -3.1% (95% CI, -4.9 to -1.3%) for CD4+, and -1.0% (95% CI, -1.8 to -0.2%) for CD8+ cells. The corresponding increase in the CD19+ cell proportion was 1.7% (95% CI, 0.4 to 3.0%). Associations were similar but slightly weaker for PM2.5. Ambient air pollution may influence the relative distribution of lymphocyte immunophenotypes of the fetus.

Early-life exposure to organophosphate pesticides and pediatric respiratory symptoms in the CHAMACOS cohort.

BACKGROUND: Although pesticide use is widespread, the possible effect of early-life exposure to organophosphate (OP) on pediatric respiratory health is not well described. OBJECTIVES: We investigated the relationship between early-life exposure to OPs and respiratory outcomes. METHODS: Participants included 359 mothers and children from the CHAMACOS birth cohort. Dialkyl phosphate (DAP) metabolites of OP pesticides, specifically diethyl (DE) and dimethyl (DM) phosphate metabolites, were measured in urine from mothers twice during pregnancy (mean = 13 and 26 weeks gestation) and from children five times during childhood (0.5-5 years). Childhood DAP concentrations were estimated by the area under curve (AUC). Mothers reported their child's respiratory symptoms at 5 and 7 years of age. We used generalized estimating equations (GEE) to examine associations of prenatal and childhood DAP concentrations with repeated measures of respiratory symptoms and exercise-induced coughing at 5 and 7 years of age, adjusting for child's sex and age, maternal smoking during pregnancy, secondhand tobacco smoke, season of birth, PM2.5, breastfeeding, mold and cockroaches in home, and distance from highway. RESULTS: Higher prenatal DAP concentrations, particularly DE, were nonsignificantly associated with respiratory symptoms in the previous 12 months at 5 or 7 years of age [adjusted odds ratio (aOR) per 10-fold increase = 1.44; 95% CI: 0.98, 2.12]. This association was strongest with total DAP and DE from the second half of pregnancy (aOR per 10-fold increase = 1.77; 95% CI: 1.06, 2.95; and 1.61; 95% CI: 1.08, 2.39, respectively). Childhood DAP, DE, and DM concentrations were associated with respiratory symptoms and exercise-induced coughing in the previous 12 months at 5 or 7 years of age (total DAPs: aOR per 10-fold increase = 2.53; 95% CI: 1.32, 4.86; and aOR = 5.40; 95% CI: 2.10, 13.91, respectively). CONCLUSIONS: Early-life exposure to OP pesticides was associated with respiratory symptoms consistent with possible asthma in childhood.

Long-term exposure to constituents of fine particulate air pollution and mortality: results from the California Teachers Study.

BACKGROUND: Several studies have reported associations between long-term exposure to ambient fine particulate matter (PM) and cardiovascular mortality. However, the health impacts of long-term exposure to specific constituents of PM(2.5) (PM with aerodynamic diameter < or = 2.5 microm) have not been explored. METHODS: We used data from the California Teachers Study, a prospective cohort of active and former female public school professionals. We developed estimates of long-term exposures to PM(2.5) and several of its constituents, including elemental carbon, organic carbon (OC), sulfates, nitrates, iron, potassium, silicon, and zinc. Monthly averages of exposure were created using pollution data from June 2002 through July 2007. We included participants whose residential addresses were within 8 and 30 km of a monitor collecting PM(2.5) constituent data. Hazard ratios (HRs) were estimated for long-term exposure for mortality from all nontraumatic causes, cardiopulmonary disease, ischemic heart disease (IHD), and pulmonary disease. RESULTS: Approximately 45,000 women with 2,600 deaths lived within 30 km of a monitor. We observed associations of all-cause, cardiopulmonary, and IHD mortality with PM(2.5) mass and each of its measured constituents, and between pulmonary mortality and several constituents. For example, for cardiopulmonary mortality, HRs for interquartile ranges of PM(2.5), OC, and sulfates were 1.55 [95% confidence interval (CI), 1.431.69], 1.80 (95% CI, 1.681.93), and 1.79 (95% CI, 1.582.03), respectively. Subsequent analyses indicated that, of the constituents analyzed, OC and sulfates had the strongest associations with all four outcomes. CONCLUSIONS: Long-term exposures to PM(2.5) and several of its constituents were associated with increased risks of all-cause and cardiopulmonary mortality in this cohort. Constituents derived from combustion of fossil fuel (including diesel), as well as those of crustal origin, were associated with some of the greatest risks. These results provide additional evidence that reduction of ambient PM(2.5) may provide significant public health benefits.

Asthma prevalence in Hispanic and Asian American ethnic subgroups: results from the California Healthy Kids Survey.

OBJECTIVES: Asthma prevalence for different ethnic groups in the United States, beyond white, black and Hispanic, is seldom reported. We compared the prevalence of asthma diagnosis among various Hispanic and Asian American ethnic subgroups using data collected from the school-based California Healthy Kids Survey. METHODS: The California Healthy Kids Survey was administered to 462 147 public school students in the seventh, ninth, and 11th grades throughout California during the 2001-2002 and 2002-2003 school years. Prevalence of lifetime asthma diagnosis was calculated for 11 Asian American Pacific Islander subgroups and 8 Hispanic subgroups. RESULTS: Asthma prevalence among Hispanic subgroups ranged from 13.2% for Mexican American students to 22.8% for Puerto Rican students and 23.0% among Cuban American students. Lifetime asthma diagnosis among the 11 Asian American Pacific Islander subgroups ranged from 10.9% among Korean American students to 23.8% among Filipino American students. CONCLUSIONS: The survey revealed substantial variation in asthma prevalence between the different Hispanic and Asian American Pacific Islander subgroups and that Pacific Islanders, Filipinos, Cubans, and Puerto Ricans are at elevated risk for asthma. Differences in the distributions of characteristics related to country of birth, residential history, generational status, and/or degree of acculturation might account for much of the observed differences in asthma prevalence between ethnic subgroups. Previous asthma prevalence estimates for Asians or Hispanics are in part a function of the particular ethnic composition of the population under investigation. We suggest that asthma studies that include a substantial number of Asian Pacific Islander and Hispanic persons use a more detailed categorization of race/ethnicity.