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BACKGROUND: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women. METHODS: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts - Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2:5 μm, ≤10 μm, and 2:5–10 μm in diameter (PM2:5, PM10, and PMcoarse, respectively); PM2:5 absorbance; nitrogen oxides (NO2 and NOx); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. RESULTS: Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM2:5 {hazard ratio (HR) =1:08 [95% confidence interval (CI): 0.77, 1.51] per 5 μg/m3 }, PM10 [1.07 (95% CI: 0.89, 1.30) per 10 μg/m3 ], PMcoarse [1.20 (95% CI: 0.96, 1.49 per 5 μg/m3 ], and NO2 [1.02 (95% CI: 0.98, 1.07 per 10 μg/m3 ], and a statistically significant association with NOx [1.04 (95% CI: 1.00, 1.08) per 20 μg/m3, p =0:04]. CONCLUSIONS: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women. © 2017, Public Health Services, US Dept of Health and Human Services. All rights reserved. Chemicals/CAS: copper, 15158-11-9, 7440-50-8; iron, 14093-02-8, 53858-86-9, 7439-89-6; nickel, 7440-02-0; nitrogen oxide, 11104-93-1; potassium, 7440-09-7; silicon, 7440-21-3; sulfur, 13981-57-2, 7704-34-9; vanadium, 7440-62-2; zinc, 7440-66-6, 14378-32-6

BackgroundDuring the last week of June 2008, central and northern California experienced thousands of forest and brush fires, giving rise to a week of severe fire-related particulate air pollution throughout the region. California experienced PM(10-2.5) (particulate matter with mass median aerodynamic diameter > 2.5 mum to < 10 mum; coarse ) and PM(2.5) (particulate matter with mass median aerodynamic diameter < 2.5 mum; fine) concentrations greatly in excess of the air quality standards and among the highest values reported at these stations since data have been collected.ObjectivesThese observations prompt a number of questions about the health impact of exposure to elevated levels of PM(10-2.5) and PM(2.5) and about the specific toxicity of PM arising from wildfires in this region.MethodsToxicity of PM(10-2.5) and PM(2.5) obtained during the time of peak concentrations of smoke in the air was determined with a mouse bioassay and compared with PM samples collected under normal conditions from the region during the month of June 2007.ResultsConcentrations of PM were not only higher during the wildfire episodes, but the PM was much more toxic to the lung on an equal weight basis than was PM collected from normal ambient air in the region. Toxicity was manifested as increased neutrophils and protein in lung lavage and by histologic indicators of increased cell influx and edema in the lung.ConclusionsWe conclude that the wildfire PM contains chemical components toxic to the lung, especially to alveolar macrophages, and they are more toxic to the lung than equal doses of PM collected from ambient air from the same region during a comparable season.

Background Air pollution data in Bangkok, Thailand, indicate that levels of particulate matter with aerodynamic diameter ≤10 μm (PM10) are significantly higher than in most cities in North America and Western Europe, where the health effects of PM10 are well documented. However, the pollution mix, seasonality, and demographics are different from those in developed Western countries. It is important, therefore, to determine whether the large metropolitan area of Bangkok is subject to similar effects of PM10. Objectives This study was designed to investigate the mortality risk from air pollution in Bangkok, Thailand. Methods The study period extended from 1999 to 2003, for which the Ministry of Public Health provided the mortality data. Measures of air pollution were derived from air monitoring stations, and information on temperature and relative humidity was obtained from the weather station in central Bangkok. The statistical analysis followed the common protocol for the multicity PAPA (Public Health and Air Pollution Project in Asia) project in using a natural cubic spline model with smooths of time and weather. Results The excess risk for non-accidental mortality was 1.3% [95% confidence interval (CI), 0.8–1.7] per 10 μg/m3 of PM10, with higher excess risks for cardiovascular and above age 65 mortality of 1.9% (95% CI, 0.8–3.0) and 1.5% (95% CI, 0.9–2.1), respectively. In addition, the effects from PM10 appear to be consistent in multipollutant models. Conclusions The results suggest strong associations between several different mortality outcomes and PM10. In many cases, the effect estimates were higher than those typically reported in Western industrialized nations.

Background A critical question regarding the association between short-term exposure to ozone and mortality is the extent to which this relationship is confounded by ambient exposure to particles. Objectives We investigated whether particulate matter < 10 and < 2.5 μm in aerodynamic diameter (PM10 and PM2.5) is a confounder of the ozone and mortality association using data for 98 U.S. urban communities from 1987 to 2000. Methods We a) estimated correlations between daily ozone and daily PM concentrations stratified by ozone or PM levels; b) included PM as a covariate in time-series models; and c) included PM as a covariate as in d), but within a subset approach considering only days with ozone below a specified value. Results Analysis was hindered by data availability. In the 93 communities with PM10 data, only 25.0% of study days had data on both ozone and PM10. In the 91 communities with PM2.5 data, only 9.2% of days in the study period had data on ozone and PM2.5. Neither PM measure was highly correlated with ozone at any level of ozone or PM. National and community-specific effect estimates of the short-term effects of ozone on mortality were robust to inclusion of PM10 or PM2.5 in time-series models. The robustness remains even at low ozone levels (< 10 ppb) using a subset approach. Conclusions Results provide evidence that neither PM10 nor PM2.5 is a likely confounder of observed ozone and mortality relationships. Further investigation is needed to investigate potential confounding of the short-term effects of ozone on mortality by PM chemical composition.

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 diameteror=10 microm) and with fine particles (PM with aerodynamic diameteror=2.5 microm) originating primarily from combustion sources. However, little is known about the relationship between HRV and coarse particles [PM with aerodynamic diameter 10-2.5 microm (PM10-2.5)], which typically result from entrainment of dust and soil or from mechanical abrasive processes in industry and transportation. We measured several HRV variables in 19 nonsmoking older adults with coronary artery disease residing in the Coachella Valley, California, a desert resort and retirement area in which ambient PM10 consists predominantly of PM10-2.5. Study subjects wore Holter monitors for 24 hr once per week for up to 12 weeks during spring 2000. Pollutant concentrations were assessed at nearby fixed-site monitors. We used mixed models that controlled for individual-specific effects to examine relationships between air pollutants and several HRV metrics. Decrements in several measures of HRV were consistently associated with both PM10 and PM10-2.5; however, there was little relationship of HRV variables with PM2.5 concentrations. The magnitude of the associations (approximately 1-4% decrease in HRV per 10-microg/m3 increase in PM10 or PM10-2.5) was comparable with those observed in several other studies of PM. Elevated levels of ambient PM10-2.5 may adversely affect HRV in older subjects with coronary artery disease.

In their article on seasonality and children’s blood lead (BPb) levels, Laidlaw et al. (2005) stated that “lead-contaminated soil in and of itself may be the primary driving mechanism of child BPb poisoning in the urban environment.” We believe that the data presented by Laidlaw et al. (2005) do not support this conclusion and that they misrepresent the many other studies of childhood lead poisoning, which support a more comprehensive, validated approach. To support their “soil-only” hypothesis, Laidlaw et al. (2005) made three primary arguments: a) soil lead represents a large and available reservoir of environmental lead; b) resuspension of lead from contaminated soil followed by inhalation of airborne particulate matter < 10 μm in diameter (PM10) and dust deposition on interior surfaces is the major source of lead exposure to children; and c) the major source of lead contaminated soil is fallout from the past use of tetraethyl lead in gasoline. Laidlaw et al. (2005) did not cite the compelling body of scientific evidence demonstrating that deteriorated lead-based paint and the contaminated dust and soil it generates is highly correlated with BPb levels in children. These have been reviewed at length elsewhere (National Academy of Sciences 1993; Jacobs 1995; President’s Task Force on Environmental Health Risks and Safety Risks to Children 2000). Indeed, Laidlaw et al. failed to recognize the enlightened statutory definition of the term “lead-based paint hazard,” which includes not only deteriorated lead-based paint but also interior settled house dust and bare soil. Together, these constitute the principal exposure sources and pathways for most (but not all) children today (Residential Lead-Based Paint Hazard Reducation Act of 1992—Title X 1992). Furthermore, documented evidence shows that soil lead levels are highest in soil at the house drip line and greatly decrease farther away from the house, regardless of whether or not the house is in a rural area or city (Jacobs 1995). Laidlaw et al. (2005) ignored confounding due to the coexistence of old, poorly maintained lead-painted housing and traffic congestion in urban areas. They failed to develop any rationale to exclude lead paint as a prominent source of lead exposure and should have included a measure of it in their models. Furthermore, they did not support their assumption that PM10 data can be used as a surrogate for airborne lead particulate. Laidlaw et al. should have used the more direct measures of airborne lead particulate levels, which are available from the U.S. Environmental Protection Agency’s (EPA) National Ambient Air Quality program (U.S. EPA 2004), rather than the convoluted indirect measures of particulate matter < 10 μm in diameter (PM10), soil moisture, and other variables. Studies of the effectiveness of soil removal in urban residential areas without addressing deteriorated lead paint have demonstrated that the “soil-only” approach being recommended by Laidlaw et al. (2005) is of limited value (U.S. EPA 1996). Even in Superfund sites where old mining and smelter wastes have resulted in very high soil lead levels, efforts that do not also address deteriorated lead paint often are disappointing. Furthermore, in the largest and most recent study of lead-based paint hazard control (which addressed lead paint hazards in > 3,000 homes in a dozen jurisdictions), house dust lead levels remained below preintervention levels for at least 3 years following the intervention (National Center for Healthy Housing and University of Cincinnati 2004). In a smaller follow-up study, dust lead levels remained between 11% and 75% lower than baseline levels for 6 years following lead-based paint hazard intervention (Wilson J, Pivetz T, Ashley P, Jacobs D, Strauss W, Menkedick J, et al., unpublished data). If the contention of Laidlaw et al. (2005) is correct (i.e., that urban soil lead is being resuspended and deposited inside homes), dust lead levels should have increased after intervention in these studies. In fact, they did not. This directly contradicts the authors’ conclusions. Finally, Laidlaw et al. (2005) erroneously cited a pooled analysis (Lanphear et al. 1998), which they believe supports their view that soil and dust lead are the most significant predictors of children’s BPb. In fact, the model used in that study also included paint lead and paint condition as variables. If the dust and soil lead terms are forced out of the model, paint lead becomes the most significant predictor, which is consistent with the now well-known pathway of paint to settled house dust and bare soil, to children’s hands, to ingestion through hand-to-mouth contact. The pooled analysis (co-authored by D.E.J.) cannot be used to justify Laidlaw et al.’s “soil-only” approach. The latest figures from the National Health and Nutrition Examination Survey indicate that the enormous disparity in the prevalence of BPb levels > 10 μg/dL once seen between African-American and white children has diminished greatly [Centers for Disease Control and Prevention (CDC) 2005]. Overall, the number of children in the United States with excessive BPb levels has declined from 890,000 in 1991–1994 to 310,000 in 1999–2002. Much of this is the result of federal, state, and local efforts to create a reservoir of lead-safe housing in communities at greatest risk. This success is tempered by recent evidence that a safe BPb level for children has not been demonstrated. The lack of a safe threshold reinforces the realization that to prevent the adverse health effects caused by lead exposure, we must exercise the wisdom to recognize and address the many sources of lead in children’s environments. The reality is too complicated and the cost of failure too devastating to reduce this to a one-source solution.

Over the last decade or so, a large number of studies have investigated the possible adverse effects of ambient air pollution on birth outcomes. We reviewed these studies, which were identified by a systematic search of the main scientific databases. Virtually all reviewed studies were population based, with information on exposure to air pollution derived from routine monitoring sources. Overall, there is evidence implicating air pollution in adverse effects on different birth outcomes, but the strength of the evidence differs between outcomes. The evidence is sufficient to infer a causal relationship between particulate air pollution and respiratory deaths in the postneonatal period. For air pollution and birth weight the evidence suggests causality, but further studies are needed to confirm an effect and its size and to clarify the most vulnerable period of pregnancy and the role of different pollutants. For preterm births and intrauterine growth retardation (IUGR) the evidence as yet is insufficient to infer causality, but the available evidence justifies further studies. Molecular epidemiologic studies suggest possible biologic mechanisms for the effect on birth weight, premature birth, and IUGR and support the view that the relation between pollution and these birth outcomes is genuine. For birth defects, the evidence base so far is insufficient to draw conclusions. In terms of exposure to specific pollutants, particulates seem the most important for infant deaths, and the effect on IUGR seems linked to polycyclic aromatic hydrocarbons, but the existing evidence does not allow precise identification of the different pollutants or the timing of exposure that can result in adverse pregnancy outcomes.

Background There is limited knowledge about the extent to which estimates of air pollution effects on health are affected by the choice for a specific exposure model. Objectives We aimed to evaluate the correlation between long-term air pollution exposure estimates using two commonly used exposure modeling techniques [dispersion and land use regression (LUR) models] and, in addition, to compare the estimates of the association between long-term exposure to air pollution and lung function in children using these exposure modeling techniques. Methods We used data of 1,058 participants of a Dutch birth cohort study with measured forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC), and peak expiratory flow (PEF) measurements at 8 years of age. For each child, annual average outdoor air pollution exposure [nitrogen dioxide (NO2), mass concentration of particulate matter with diameters ≤ 2.5 and ≤ 10 μm (PM2.5, PM10), and PM2.5 soot] was estimated for the current addresses of the participants by a dispersion and a LUR model. Associations between exposures to air pollution and lung function parameters were estimated using linear regression analysis with confounder adjustment. Results Correlations between LUR- and dispersion-modeled pollution concentrations were high for NO2, PM2.5, and PM2.5 soot (R = 0.86–0.90) but low for PM10 (R = 0.57). Associations with lung function were similar for air pollutant exposures estimated using LUR and dispersion modeling, except for associations of PM2.5 with FEV1 and FVC, which were stronger but less precise for exposures based on LUR compared with dispersion model. Conclusions Predictions from LUR and dispersion models correlated very well for PM2.5, NO2, and PM2.5 soot but not for PM10. Health effect estimates did not depend on the type of model used to estimate exposure in a population of Dutch children. Citation Wang M, Gehring U, Hoek G, Keuken M, Jonkers S, Beelen R, Eeftens M, Postma DS, Brunekreef B. 2015. Air pollution and lung function in Dutch children: a comparison of exposure estimates and associations based on land use regression and dispersion exposure modeling approaches. Environ Health Perspect 123:847–851; http://dx.doi.org/10.1289/ehp.1408541

Background Short-term exposure to air pollution has adverse effects among patients with asthma, but whether long-term exposure to air pollution is a cause of adult-onset asthma is unclear. Objective We aimed to investigate the association between air pollution and adult onset asthma. Methods Asthma incidence was prospectively assessed in six European cohorts. Exposures studied were annual average concentrations at home addresses for nitrogen oxides assessed for 23,704 participants (including 1,257 incident cases) and particulate matter (PM) assessed for 17,909 participants through ESCAPE land-use regression models and traffic exposure indicators. Meta-analyses of cohort-specific logistic regression on asthma incidence were performed. Models were adjusted for age, sex, overweight, education, and smoking and included city/area within each cohort as a random effect. Results In this longitudinal analysis, asthma incidence was positively, but not significantly, associated with all exposure metrics, except for PMcoarse. Positive associations of borderline significance were observed for nitrogen dioxide [adjusted odds ratio (OR) = 1.10; 95% CI: 0.99, 1.21 per 10 μg/m3; p = 0.10] and nitrogen oxides (adjusted OR = 1.04; 95% CI: 0.99, 1.08 per 20 μg/m3; p = 0.08). Nonsignificant positive associations were estimated for PM10 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 10 μg/m3), PM2.5 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 5 μg/m3), PM2.5absorbance (adjusted OR = 1.06; 95% CI: 0.95, 1.19 per 10–5/m), traffic load (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 4 million vehicles × meters/day on major roads in a 100-m buffer), and traffic intensity (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 5,000 vehicles/day on the nearest road). A nonsignificant negative association was estimated for PMcoarse (adjusted OR = 0.98; 95% CI: 0.87, 1.14 per 5 μg/m3). Conclusions Results suggest a deleterious effect of ambient air pollution on asthma incidence in adults. Further research with improved personal-level exposure assessment (vs. residential exposure assessment only) and phenotypic characterization is needed. Citation Jacquemin B, Siroux V, Sanchez M, Carsin AE, Schikowski T, Adam M, Bellisario V, Buschka A, Bono R, Brunekreef B, Cai Y, Cirach M, Clavel-Chapelon F, Declercq C, de Marco R, de Nazelle A, Ducret-Stich RE, Ferretti VV, Gerbase MW, Hardy R, Heinrich J, Janson C, Jarvis D, Al Kanaani Z, Keidel D, Kuh D, Le Moual N, Nieuwenhuijsen MJ, Marcon A, Modig L, Pin I, Rochat T, Schindler C, Sugiri D, Stempfelet M, Temam S, Tsai MY, Varraso R, Vienneau D, Vierkötter A, Hansell AL, Krämer U, Probst-Hensch NM, Sunyer J, Künzli N, Kauffmann F. 2015. Ambient air pollution and adult asthma incidence in six European cohorts (ESCAPE). Environ Health Perspect 123:613–621; http://dx.doi.org/10.1289/ehp.1408206

Background: Although serious health effects associated with particulate matter (PM) with aerodynamic diameter ≤ 10 μm (PM10) and ≤ 2.5 μm (PM2.5; fine fraction) are documented in many studies, the effects of coarse PM (PM2.5–10) are still under debate. Objective: In this study, we estimated the effects of short-term exposure of PM2.5–10 on daily mortality in Stockholm, Sweden. Method: We collected data on daily mortality for the years 2000 through 2008. Concentrations of PM10, PM2.5, ozone, and carbon monoxide were measured simultaneously in central Stockholm. We used additive Poisson regression models to examine the association between daily mortality and PM2.5–10 on the day of death and the day before. Effect estimates were adjusted for other pollutants (two-pollutant models) during different seasons. Results: We estimated a 1.68% increase [95% confidence interval (CI): 0.20%, 3.15%] in daily mortality per 10-μg/m3 increase in PM2.5–10 (single-pollutant model). The association with PM2.5–10 was stronger for November through May, when road dust is most important (1.69% increase; 95% CI: 0.21%, 3.17%), compared with the rest of the year (1.31% increase; 95% CI: –2.08%, 4.70%), although the difference was not statistically significant. When adjusted for other pollutants, particularly PM2.5, the effect estimates per 10 μg/m3 for PM2.5–10 decreased slightly but were still higher than corresponding effect estimates for PM2.5. Conclusions: Our analysis shows an increase in daily mortality associated with elevated urban background levels of PM2.5–10. Regulation of PM2.5–10 should be considered, along with actions to specifically reduce PM2.5–10 emissions, especially road dust suspension, in cities.

Background Several studies suggest that airborne particulate matter (PM) is associated with infant mortality; however, most focused on short-term exposure to larger particles. Objectives We evaluated associations between long-term exposure to different sizes of particles [total suspended particles (TSP), PM ≤ 10 μm in aerodynamic diameter (PM10), ≤ 10–2.5 μm (PM10–2.5), and ≤ 2.5 μm (PM2.5)] and infant mortality in a cohort in Seoul, Korea, 2004–2007. Methods The study includes 359,459 births with 225 deaths. We applied extended Cox proportional hazards modeling with time-dependent covariates to three mortality categories: all causes, respiratory, and sudden infant death syndrome (SIDS). We calculated exposures from birth to death (or end of eligibility for outcome at 1 year of age) and pregnancy (gestation and each trimester) and treated exposures as time-dependent variables for subjects’ exposure for each pollutant. We adjusted by sex, gestational length, season of birth, maternal age and educational level, and heat index. Each cause of death and exposure time frame was analyzed separately. Results We found a relationship between gestational exposures to PM and infant mortality from all causes or respiratory causes for normal-birth-weight infants. For total mortality (all causes), risks were 1.44 (95% confidence interval, 1.06–1.97), 1.65 (1.18–2.31), 1.53 (1.22–1.90), and 1.19 (0.83–1.70) per interquartile range increase in TSP, PM10, PM2.5, and PM10–2.5, respectively; for respiratory mortality, risks were 3.78 (1.18–12.13), 6.20 (1.50–25.66), 3.15 (1.26–7.85), and 2.86 (0.76–10.85). For SIDS, risks were 0.92 (0.33–2.58), 1.15 (0.38–3.48), 1.42 (0.71–2.87), and 0.57 (0.16–1.96), respectively. Conclusions Our findings provide supportive evidence of an association of long-term exposure to PM air pollution with infant mortality.

In their paper, Bell et al. (2007) examined the effects of ambient air pollutants on birth weight in children born in Connecticut and Massachusetts between 1999 and 2002. The study is the largest among the studies conducted in the United States and has provided evidence that, even with pollutant levels that met the air quality standards, significant reductions in birth weight occurred. The study findings are in line with other articles; however, there are several concerns that need further attention. Infants with preterm birth (born at 32–37 weeks of gestation) were included in the analysis, and this may have affected the overall and the third trimester–specific results. Although these children comprised only 6.7% of the sample, their birth weights were greatly affected (i.e., mean birth weight was 585–1,050 g less than those born at 39–40 weeks of gestation). In the discussion, Bell et al. (2007) pointed out that the effect of air pollutants on birth weight could be mediated by the effect of these pollutants on preterm birth and/or on fetal growth. It is unclear whether the effects observed in this study were mediated by one or both competing mechanisms. Bell et al.’s Table 6 compared studies that tested pollutant effects mediated only by fetal growth (Basu et al. 2004; Parker et al. 2005; Ritz and Yu 1999; Salam et al. 2005), only by preterm birth (Rogers and Dunlop 2006; Rogers et al. 2000), or by both mechanisms separately (Wilhelm and Ritz 2003, 2005; Woodruff et al. 2003). Bell et al. (2007) could have further benefited readers if they had evaluated pollutant effects on intrauterine growth restriction (IUGR), a metric of pathological fetal growth. Although IUGR is conventionally defined based on the bottom 10th percentile of the birth weight distribution, a better approach would be to define it by < 15th percentile of predicted birth weight based on gestational age, infant sex, and maternal race. Pollutant data were not available from all counties. As such, different counties contributed to different exposure effects. This makes the comparison between single and two-pollutant models difficult. In Figure 2 (Bell et al. 2007), for example, the effect of particulate matter < 2.5 μm in aerodynamic diameter (PM2.5; measured in 13 counties) seems to have been significantly changed when adjusted for carbon monoxide (measured in 7 counties). It would have been more meaningful if sensitivity analyses were conducted comparing one and two-pollutant models restricting to those counties that had data on all exposures. The detrimental effect of PM2.5 on birth weight was significantly larger in black infants than in white infants. Hispanic white infants were at increased risk of low birth weight in a similar population (Maisonet et al. 2001). Thus, combining non-Hispanic and Hispanic whites into one group, it is not possible to determine whether Hispanic infants were disproportionately affected by ambient pollutants. There is significant heterogeneity in the percentages of African-American and Hispanic white population by county (U.S. Census Bureau 2007). For example, within the state of Massachusetts, 25% of residents were African American and about 18% were Hispanic in Suffolk, whereas about 2% each were African American and Hispanic in Barnstable. In addition, in counties with higher proportions of African-American and Hispanic populations, the percentages living in poverty were also much higher. Although Bell et al. (2007) acknowledged within-county heterogeneity, questions remain about whether significant heterogeneity in effects existed across counties. In summary, the results would have been more appealing if Bell et al. (2007) could provide data to show whether pollutant effects were mediated by preterm birth and/or affected fetal growth, and whether these effects were greater in Hispanics, in mothers who smoked, and in counties with a higher proportion of people living in poverty.

About half the world’s population relies on biomass fuels as the primary domestic energy source (Smith et al. 2004). In rural China, biomass fuels account for about 80% of domestic energy (World Resources Institute 1998). Biomass combustion results in severe indoor air pollution, especially particulate matter (PM). Exposure to PM has been associated with increased risk for a suite of negative health outcomes, such as acute respiratory infection, chronic respiratory disease, and mortality (U.S. Environmental Protection Agency 2004). The Chinese population suffers a high health burden from lung diseases, and respiratory disease is the primary cause of death in rural China (Schmidt 2002). Indoor PM from biomass fuels is one of the most serious yet least studied environmental health problems in China. In fact, little is known about human exposure to indoor PM in China and how different populations may be affected. Data are particularly lacking for rural China (Schmidt 2002). Several studies conducted in other parts of the world have investigated exposures to indoor air pollution from biomass fuels, finding that exposure patterns differed by sex, location in the home, and activity patterns (e.g., cooking vs. noncooking) (Balakrishnan et al. 2002; Ezzati et al. 2000). Indoor air pollution in China has been explored in several previous studies. Respirable particles [RPM; PM with a median aerodynamic diameter ≤ 4 μm (PM4)], carbon monoxide, and sulfur dioxide were measured using stationary monitors at the household level in four Chinese provinces. The two provinces using biomass as the primary fuel had the highest PM4 concentrations (Jin et al. 2005). He et al. (2005) monitored multiple pollutants (PM4, CO, SO2, fluoride, and arsenic) at four points inside homes consuming coals and/or biomass fuels in the Guizhou and Shaanxi provinces. PM4 was higher in Guizhou households than in those in Shaanxi because of the fuel and stove combination (i.e., biomass fuel instead of coal, traditional stove instead of improved stove). Wang et al. (2006) investigated PM with an aerodynamic diameter ≤ 10 μm (PM10), PM with an aerodynamic diameter ≤ 2.5 μm (PM2.5), and 18 PM2.5 chemical components in four hospitals and adjacent outdoor environments in Guangzhou, China. Indoor PM2.5 levels in the hospitals were significantly higher than the U.S. Environmental Protection Agency ambient PM2.5 standard. Additional summaries of research on exposure to indoor air pollution in China are provided elsewhere (Mestl et al. 2007a; Sinton et al. 1995). Despite these important studies, several unanswered questions remain. Specifically, estimates of indoor PM exposure typically were based on stationary monitors, often in combination with daily activity dairies, rather than continuous personal PM monitoring. Time–activity patterns were recorded by participants rather than researchers, introducing potential bias. Published studies do not include time–activity data for mainland China. In addition, monitoring generally applied exposure metrics of daily or hourly values and therefore has been unable to illuminate heterogeneity in exposure at smaller time scales. Finally, with the notable exception of Wang et al. (2006), most studies focused on PM10 or PM4 rather than PM2.5, although PM2.5 appears to be more closely linked to adverse health effects. In this study we investigated indoor PM10 and PM2.5 levels in northeastern China using stationary and personal monitoring and time–activity diaries generated by direct observation. We compared exposures for cooks and noncooks, indoor and outdoor levels, urban and rural homes, and fuel type. Personal monitoring data include second-by-second measurements, allowing analysis of variation at small time scales. To the best of our knowledge, this is the first study to employ personal PM2.5 monitoring to assess individual exposures in China. In addition, we believe this study to be one of the first in mainland China to collect time–activity data.

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.

We examined the relationship between intrapulmonary particle distribution of carbonaceous and mineral dusts and remodeling of the airways along anatomically distinct airway paths in the lungs of Hispanic males from the central valley of California. Lung autopsy specimens from the Fresno County Coroner's Office were prepared by intratracheal instillation of 2% glutaraldehyde at 30 cm H(2)O pressure. Two distinct airway paths into the apico-posterior and apico-anterior portions of the left upper lung lobe were followed. Tissue samples for histologic analysis were generally taken from the intrapulmonary second, fourth, sixth, and ninth airway generations. Parenchymal tissues beyond the 12th airway generation of each airway path were also analyzed. There was little evidence of visible particle accumulation in the larger conducting airways (generations 2-6), except in bronchial-associated lymphoid tissues and within peribronchial connective tissue. In contrast, terminal and respiratory bronchioles arising from each pathway revealed varying degrees of wall thickening and remodeling. Walls with marked thickening contained moderate to heavy amounts of carbonaceous and mineral dusts. Wall thickening was associated with increases in collagen and interstitial inflammatory cells, including dust-laden macrophages. These changes were significantly greater in first-generation respiratory bronchioles compared to second- and third-generation respiratory bronchioles. These findings suggest that accumulation of carbonaceous and mineral dust in the lungs is significantly affected by lung anatomy with the greatest retention in centers of lung acini. Furthermore, there is significant remodeling of this transitional zone in humans exposed to ambient particulate matter.