Effect of Early Life Exposure to Air Pollution on Development of Childhood Asthma

Background

There is increasing recognition of the importance of early environmental exposures in the development of childhood asthma. Outdoor air pollution is a recognized asthma trigger, but it is unclear whether exposure influences incident disease. We investigated the effect of exposure to ambient air pollution in utero and during the first year of life on risk of subsequent asthma diagnosis in a population-based nested case–control study.

Methods

We assessed all children born in southwestern British Columbia in 1999 and 2000 (n = 37,401) for incidence of asthma diagnosis up to 3–4 years of age using outpatient and hospitalization records. Asthma cases were age- and sex-matched to five randomly chosen controls from the eligible cohort. We estimated each individual’s exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data as well as land use regression models adjusted for temporal variation. We used logistic regression analyses to estimate effects of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter ≤ 10 μm and ≤ 2.5 μm in aerodynamic diameter (PM₁₀ and PM_2.5), ozone, sulfur dioxide, black carbon, woodsmoke, and proximity to roads and point sources on asthma diagnosis.

Results

A total of 3,482 children (9%) were classified as asthma cases. We observed a statistically significantly increased risk of asthma diagnosis with increased early life exposure to CO, NO, NO₂, PM₁₀, SO₂, and black carbon and proximity to point sources. Traffic-related pollutants were associated with the highest risks: adjusted odds ratio = 1.08 (95% confidence interval, 1.04–1.12) for a 10-μg/m³ increase of NO, 1.12 (1.07–1.17) for a 10-μg/m³ increase in NO₂, and 1.10 (1.06–1.13) for a 100-μg/m³ increase in CO. These data support the hypothesis that early childhood exposure to air pollutants plays a role in development of asthma.     

Respiratory Disease in Relation to Outdoor Air Pollution in Kanpur,India

ABSTRACT

This paper examines the effect of outdoor air pollution on respiratory disease in Kanpur, India, based on data from 2006. Exposure to air pollution is represented by annual emissions of sulfur dioxide (SO₂), particulate matter (PM), and nitrogen oxides (NO_x) from 11 source categories, established as a geographic information system (GIS)-based emission inventory in 2 km × 2 km grid. Respiratory disease is represented by number of patients who visited specialist pulmonary hospital with symptoms of respiratory disease. The results showed that (1) the main sources of air pollution are industries, domestic fuel burning, and vehicles; (2) the emissions of PM per grid are strongly correlated to the emissions of SO₂ and NO_x; and (3) there is a strong correlation between visits to a hospital due to respiratory disease and emission strength in the area of residence. These results clearly indicate that appropriate health and environmental monitoring, actions to reduce emissions to air, and further studies that would allow assessing the development in health status are necessary.

[Supplementary materials are available for this article. Go to the publisher's online edition of Archives of Environmental & Occupational Health for material on emission of SO₂, PM, NO_x from various sources, and total number of inhabitants, total number of patients in grid squares covering the Kanpur city.]     

Air Pollution,Aeroallergens, and Emergency Room Visits for Acute Respiratory Diseases and Gastroenteric Disorders among Young Children in Six Italian Cities

Background

Past studies reported evidence of associations between air pollution and respiratory symptoms and morbidity for children. Few studies examined associations between air pollution and emergency room (ER) visits for wheezing, and even fewer for gastroenteric illness. We conducted a multicity analysis of the relationship between air pollution and ER visits for wheezing and gastroenteric disorder in children 0–2 years of age.

Methods

We obtained ER visit records for wheezing and gastroenteric disorder from six Italian cities. A city-specific case–crossover analysis was applied to estimate effects of particulate matter (PM), nitrogen dioxide, sulfur dioxide, ozone, and carbon monoxide, adjusting for immediate and delayed effects of temperature. Lagged effects of air pollutants up to 6 prior days were examined. The city-specific results were combined using a random-effect meta-analysis.

Results

CO and SO₂ were most strongly associated with wheezing, with a 2.7% increase [95% confidence interval (CI), 0.5–4.9] for a 1.04-μg/m³ increase in 7-day average CO and a 3.4% (95% CI, 1.5–5.3) increase for an 8.0-μg/m³ increase in SO₂. Positive associations were also found for PM with aerodynamic diameter ≤ 10 μg and NO₂. We found a significant association between the 3-day moving average CO and gastroenteric disorders [3.8% increase (95% CI, 1.0–6.8)]. When data were stratified by season, the associations were stronger in summer for wheezing and in winter for gastroenteric disorders.

Conclusion

Air pollution is associated with triggering of wheezing and gastroenteric disorders in children 0–2 years of age; more work is needed to understand the mechanisms to help prevent wheezing in children.     

Residential traffic-related pollution exposures and exhaled nitric oxide in the children's health study

Background: The fractional concentration of nitric oxide in exhaled air (Fe_NO) potentially detects airway inflammation related to air pollution exposure. Existing studies have not yet provided conclusive evidence on the association of Fe_NO with traffic-related pollution (TRP).Objectives: We evaluated the association of Fe_NO with residential TRP exposure in a large cohort of children.Methods: We related Fe_NO measured on 2,143 children (ages 7–11 years) who participated in the Southern California Children’s Health Study (CHS) to five classes of metrics of residential TRP: distances to freeways and major roads; length of all and local roads within circular buffers around the home; traffic densities within buffers; annual average line source dispersion modeled nitrogen oxides (NO_x) from freeways and nonfreeway roads; and predicted annual average nitrogen oxide, nitrogen dioxide, and NO_x from a model based on intracommunity sampling in the CHS.Results: In children with asthma, length of roads was positively associated with Fe_NO, with stronger associations in smaller buffers [46.7%; 95% confidence interval (CI), 14.3–88.4], 12.4% (95% CI, –8.8 to 38.4), and 4.1% (95% CI, –14.6 to 26.8) higher Fe_NO for 100-, 300-, and 1,000-m increases in the length of all roads in 50-, 100-, and 200-m buffers, respectively. Other TRP metrics were not significantly associated with Fe_NO, even though the study design was powered to detect exposures explaining as little as 0.4% of the variation in natural log-transformed Fe_NO (R² = 0.004).Conclusion: Length of road was the only indicator of residential TRP exposure associated with airway inflammation in children with asthma, as measured by Fe_NO.     

Mortality in Young Adults following in Utero and Childhood Exposure to Arsenic in Drinking Water

Background: Beginning in 1958, the city of Antofagasta in northern Chile was exposed to high arsenic concentrations (870 µg/L) when it switched water sources. The exposure abruptly stopped in 1970 when an arsenic-removal plant commenced operations. A unique exposure scenario like this—with an abrupt start, clear end, and large population (125,000 in 1970), all with essentially the same exposure—is rare in environmental epidemiology. Evidence of increased mortality from lung cancer, bronchiectasis, myocardial infarction, and kidney cancer has been reported among young adults who were in utero or children during the high-exposure period.Objective: We investigated other causes of mortality in Antofagasta among 30- to 49-year-old adults who were in utero or ≤ 18 years of age during the high-exposure period.Methods: We compared mortality data between Antofagasta and the rest of Chile for people 30–49 years of age during 1989–2000. We estimated expected deaths from mortality rates in all of Chile, excluding Region II where Antofagasta is located, and calculated standardized mortality ratios (SMRs).Results: We found evidence of increased mortality from bladder cancer [SMR = 18.1; 95% confidence interval (CI): 11.3, 27.4], laryngeal cancer (SMR = 8.1; 95% CI: 3.5, 16.0), liver cancer (SMR = 2.5; 95% CI: 1.6, 3.7), and chronic renal disease (SMR = 2.0; 95% CI: 1.5, 2.8).Conclusions: Taking together our findings in the present study and previous evidence of increased mortality from other causes of death, we conclude that arsenic in Antofagasta drinking water has resulted in the greatest increases in mortality in adults < 50 years of age ever associated with early-life environmental exposure.     

Early-Life Respiratory Infections in Infants with Cow’s Milk Allergy: An Expert Opinion on the Available Evidence and Recommendations for Future Research

Acute respiratory infections are a common cause of morbidity in infants and young children. This high rate of respiratory infections in early life has a major impact on healthcare resources and antibiotic use, with the associated risk of increasing antibiotic resistance, changes in intestinal microbiota composition and activity and, consequently, on the future health of children. An international group of clinicians and researchers working in infant nutrition and cow’s milk allergy (CMA) met to review the available evidence on the prevalence of infections in healthy infants and in those with allergies, particularly CMA; the factors that influence susceptibility to infection in early life; links between infant feeding, CMA and infection risk; and potential strategies to modulate the gut microbiota and infection outcomes. The increased susceptibility of infants with CMA to infections, and the reported potential benefits with prebiotics, probiotics and synbiotics with regard to improving infection outcomes and reducing antibiotic usage in infants with CMA, makes this a clinically important issue that merits further research.     

Association between GIS-Based Exposure to Urban Air Pollution during Pregnancy and Birth Weight in the INMA Sabadell Cohort

Background

There is growing evidence that traffic-related air pollution reduces birth weight. Improving exposure assessment is a key issue to advance in this research area.

Objective

We investigated the effect of prenatal exposure to traffic-related air pollution via geographic information system (GIS) models on birth weight in 570 newborns from the INMA (Environment and Childhood) Sabadell cohort.

Methods

We estimated pregnancy and trimester-specific exposures to nitrogen dioxide and aromatic hydrocarbons [benzene, toluene, ethylbenzene, m/p-xylene, and o-xylene (BTEX)] by using temporally adjusted land-use regression (LUR) models. We built models for NO₂ and BTEX using four and three 1-week measurement campaigns, respectively, at 57 locations. We assessed the relationship between prenatal air pollution exposure and birth weight with linear regression models. We performed sensitivity analyses considering time spent at home and time spent in nonresidential outdoor environments during pregnancy.

Results

In the overall cohort, neither NO₂ nor BTEX exposure was significantly associated with birth weight in any of the exposure periods. When considering only women who spent < 2 hr/day in nonresidential outdoor environments, the estimated reductions in birth weight associated with an interquartile range increase in BTEX exposure levels were 77 g [95% confidence interval (CI), 7–146 g] and 102 g (95% CI, 28–176 g) for exposures during the whole pregnancy and the second trimester, respectively. The effects of NO₂ exposure were less clear in this subset.

Conclusions

The association of BTEX with reduced birth weight underscores the negative role of vehicle exhaust pollutants in reproductive health. Time–activity patterns during pregnancy complement GIS-based models in exposure assessment.     

From Good Intentions to Proven Interventions: Effectiveness of Actions to Reduce the Health Impacts of Air Pollution

Background

Associations between air pollution and a multitude of health effects are now well established. Given ubiquitous exposure to some level of air pollution, the attributable health burden can be high, particularly for susceptible populations.

Objectives

An international multidisciplinary workshop was convened to discuss evidence of the effectiveness of actions to reduce health impacts of air pollution at both the community and individual level. The overall aim was to summarize current knowledge regarding air pollution exposure and health impacts leading to public health recommendations.

Discussion

During the workshop, experts reviewed the biological mechanisms of action of air pollution in the initiation and progression of disease, as well as the state of the science regarding community and individual-level interventions. The workshop highlighted strategies to reduce individual baseline risk of conditions associated with increased susceptibility to the effects of air pollution and the need to better understand the role of exposure duration in disease progression, reversal, and adaptation.

Conclusion

We have identified two promising and largely unexplored strategies to address and mitigate air pollution–related health impacts: reducing individual baseline risk of cardiovascular disease and incorporating air pollution–related health impacts into land-use decisions.     

A Framework for Examining Social Stress and Susceptibility to Air Pollution in Respiratory Health

Objective

There is growing interest in disentangling the health effects of spatially clustered social and physical environmental exposures and in exploring potential synergies among them, with particular attention directed to the combined effects of psychosocial stress and air pollution. Both exposures may be elevated in lower-income urban communities, and it has been hypothesized that stress, which can influence immune function and susceptibility, may potentiate the effects of air pollution in respiratory disease onset and exacerbation. In this paper, we attempt to synthesize the relevant research from social and environmental epidemiology, toxicology, immunology, and exposure assessment to provide a useful framework for environmental health researchers aiming to investigate the health effects of environmental pollution in combination with social or psychological factors.

Data synthesis

We review the existing epidemiologic and toxicologic evidence on synergistic effects of stress and pollution, and then describe the physiologic effects of stress and key issues related to measuring and evaluating stress as it relates to physical environmental exposures and susceptibility. Finally, we identify some of the major methodologic challenges ahead as we work toward disentangling the health effects of clustered social and physical exposures and accurately describing the interplay among these exposures.

Conclusions

There is still tremendous work to be done toward understanding the combined and potentially synergistic health effects of stress and pollution. As this research proceeds, we recommend careful attention to the relative temporalities of stress and pollution exposures, to nonlinearities in their independent and combined effects, to physiologic pathways not elucidated by epidemiologic methods, and to the relative spatial distributions of social and physical exposures at multiple geographic scales.     

Differential DNA Methylation in Umbilical Cord Blood of Infants Exposed to Low Levels of Arsenic in Utero

Background: There is increasing epidemiologic evidence that arsenic exposure in utero, even at low levels found throughout much of the world, is associated with adverse reproductive outcomes and may contribute to long-term health effects. Animal models, in vitro studies, and human cancer data suggest that arsenic may induce epigenetic alterations, specifically by altering patterns of DNA methylation.Objectives: In this study we aimed to identify differences in DNA methylation in cord blood samples of infants with in utero, low-level arsenic exposure.Methods: DNA methylation of cord-blood derived DNA from 134 infants involved in a prospective birth cohort in New Hampshire was profiled using the Illumina Infinium Methylation450K array. In utero arsenic exposure was estimated using maternal urine samples collected at 24–28 weeks gestation. We used a novel cell mixture deconvolution methodology for examining the association between inferred white blood cell mixtures in infant cord blood and in utero arsenic exposure; we also examined the association between methylation at individual CpG loci and arsenic exposure levels.Results: We found an association between urinary inorganic arsenic concentration and the estimated proportion of CD8⁺ T lymphocytes (1.18; 95% CI: 0.12, 2.23). Among the top 100 CpG loci with the lowest p-values based on their association with urinary arsenic levels, there was a statistically significant enrichment of these loci in CpG islands (p = 0.009). Of those in CpG islands (n = 44), most (75%) exhibited higher methylation levels in the highest exposed group compared with the lowest exposed group. Also, several CpG loci exhibited a linear dose-dependent relationship between methylation and arsenic exposure.Conclusions: Our findings suggest that in utero exposure to low levels of arsenic may affect the epigenome. Long-term follow-up is planned to determine whether the observed changes are associated with health outcomes.     

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.     

Common Genetic Variation,Residential Proximity to Traffic Exposure,and Left Ventricular Mass: The Multi-Ethnic Study of Atherosclerosis

Background

Elevated left ventricular mass (LVM) is a strong predictor of negative cardiovascular outcomes, including heart failure, stroke, and sudden cardiac death. A relationship between close (< 50 m compared with > 150 m) residential proximity to major roadways and higher LVM has previously been described, but the mechanistic pathways that are involved in this relationship are not known. Understanding genetic factors that influence susceptibility to these effects may provide insight into relevant mechanistic pathways.

Objective

We set out to determine whether genetic polymorphisms in genes affecting vascular and autonomic function, blood pressure, or inflammation influence the relationship between traffic proximity and LVM.

Methods

This was a cross-sectional study of 1,376 genotyped participants in the Multi-Ethnic Study of Atherosclerosis, with cardiac magnetic resonance imaging performed between 2000 and 2002. The impact of tagged single-nucleotide polymorphisms (tagSNPs) and inferred haplotypes in 12 candidate genes (ACE, ADRB2, AGT, AGTR1, ALOX15, EDN1, GRK4, PTGS1, PTGS2, TLR4, VEGFA, and VEGFB) on the relationship between residential proximity to major roadways and LVM was analyzed using multiple linear regression, adjusting for multiple potential confounders.

Results

After accounting for multiple testing and comparing homozygotes, tagSNPs in the type 1 angiotensin II receptor (AGTR1, rs6801836) and arachidonate 15-lipoxygenase (ALOX15, rs2664593) genes were each significantly (q < 0.2) associated with a 9–10% difference in the association between residential proximity to major roadways and LVM. Participants with suboptimal blood pressure control demonstrated stronger interactions between AGTR1 and traffic proximity.

Conclusions

Common polymorphisms in genes responsible for vascular function, inflammation, and oxidative stress appear to modify associations between proximity to major roadways and LVM. Further understanding of how genes modify effects of air pollution on CVD may help guide research efforts into specific mechanistic pathways.     

Risk-Based Prioritization among Air Pollution Control Strategies in the Yangtze River Delta,China

Background

The Yangtze River Delta (YRD) in China is a densely populated region with recent dramatic increases in energy consumption and atmospheric emissions.

Objectives

We studied how different emission sectors influence population exposures and the corresponding health risks, to inform air pollution control strategy design.

Methods

We applied the Community Multiscale Air Quality (CMAQ) Modeling System to model the marginal contribution to baseline concentrations from different sectors. We focused on nitrogen oxide (NO_x) control while considering other pollutants that affect fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] and ozone concentrations. We developed concentration–response (C-R) functions for PM_2.5 and ozone mortality for China to evaluate the anticipated health benefits.

Results

In the YRD, health benefits per ton of emission reductions varied significantly across pollutants, with reductions of primary PM_2.5 from the industry sector and mobile sources showing the greatest benefits of 0.1 fewer deaths per year per ton of emission reduction. Combining estimates of health benefits per ton with potential emission reductions, the greatest mortality reduction of 12,000 fewer deaths per year [95% confidence interval (CI), 1,200–24,000] was associated with controlling primary PM_2.5 emissions from the industry sector and reducing sulfur dioxide (SO₂) from the power sector, respectively. Benefits were lower for reducing NO_x emissions given lower consequent reductions in the formation of secondary PM_2.5 (compared with SO₂) and increases in ozone concentrations that would result in the YRD.

Conclusions

Although uncertainties related to C-R functions are significant, the estimated health benefits of emission reductions in the YRD are substantial, especially for sectors and pollutants with both higher health benefits per unit emission reductions and large potential for emission reductions.     

The Public Health and Air Pollution in Asia (PAPA) Project: estimating the mortality effects of particulate matter in Bangkok, Thailand

BACKGROUND: Air pollution data in Bangkok, Thailand, indicate that levels of particulate matter with aerodynamic diameter < or = 10 microm (PM(10)) are significantly higher than in most cities in North America and Western Europe, where the health effects of PM(10) 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 PM(10). 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 microg/m(3) of PM(10), 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 PM(10) appear to be consistent in multipollutant models. CONCLUSIONS: The results suggest strong associations between several different mortality outcomes and PM(10). In many cases, the effect estimates were higher than those typically reported in Western industrialized nations.     

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.     

Ambient particulate matter air pollution and venous thromboembolism in the Women's Health Initiative Hormone Therapy trials

Background

The putative effects of postmenopausal hormone therapy on the association between particulate matter (PM) air pollution and venous thromboembolism (VTE) have not been assessed in a randomized trial of hormone therapy, despite its widespread use among postmenopausal women.

Objective

In this study, we examined whether hormone therapy modifies the association of PM with VTE risk.

Methods

Postmenopausal women 50–79 years of age (n = 26,450) who did not have a history of VTE and who were not taking anticoagulants were enrolled in the Women’s Health Initiative Hormone Therapy trials at 40 geographically diverse U.S. clinical centers. The women were randomized to treatment with estrogen versus placebo (E trial) or to estrogen plus progestin versus placebo (E + P trial). We used age-stratified Cox proportional hazard models to examine the association between time to incident, centrally adjudicated VTE, and daily mean PM concentrations spatially interpolated at geocoded addresses of the participants and averaged over 1, 7, 30, and 365 days.

Results

During the follow-up period (mean, 7.7 years), 508 participants (2.0%) had VTEs at a rate of 2.6 events per 1,000 person-years. Unadjusted and covariate-adjusted VTE risk was not associated with concentrations of PM < 2.5 μm (PM_2.5) or < 10 μm (PM₁₀)] in aerodynamic diameter and PM × active treatment interactions were not statistically significant (p > 0.05) regardless of PM averaging period, either before or after combining data from both trials [e.g., combined trial-adjusted hazard ratios (95% confidence intervals) per 10 μg/m³ increase in annual mean PM_2.5 and PM₁₀, were 0.93 (0.54–1.60) and 1.05 (0.72–1.53), respectively]. Findings were insensitive to alternative exposure metrics, outcome definitions, time scales, analytic methods, and censoring dates.

Conclusions

In contrast to prior research, our findings provide little evidence of an association between short-term or long-term PM exposure and VTE, or clinically important modification by randomized exposure to exogenous estrogens among postmenopausal women.     

Indoor Air Pollution from Biomass Combustion and its Adverse Health Effects in Central India: An Exposure-Response Study

Background:

Some of the highest exposures to air pollutants in developing countries occur inside homes where biofuels are used for daily cooking. Inhalation of these pollutants may cause deleterious effects on health.

Objectives:

To assess the respiratory and other morbidities associated with use of various types of cooking fuels in rural area of Nagpur and to study the relationship between the duration of exposure (exposure index [EI]) and various morbidities.

Materials and Methods:

A total of 760 non-smoking, non-pregnant women aged 15 years and above (mean age 32.51 ΁ 14.90 years) exposed to domestic smoke from cooking fuels from an early age, working in poorly ventilated kitchen were selected and on examination presented with various health problems. Exposure was calculated as the average hours spent daily for cooking multiplied by the number of years. Symptoms were enquired by means of a standard questionnaire adopted from that of the British Medical Research Council. Lung function was assessed by the measurement of peak expiratory flow rate (PEFR). PEFR less than 80% of the predicted was considered as abnormal pulmonary function.

Results and Conclusions:

Symptoms like eye irritation, headache, and diminution of vision were found to be significantly higher in biomass users (P < 0.05). Abnormal pulmonary function, chronic bronchitis, and cataract in biomass users was significantly higher than other fuel users (P < 0.05). Moreover an increasing trend in prevalence of symptoms/morbid conditions was observed with increase in EI. The presence of respiratory symptoms/morbid conditions was associated with lower values of both observed and percent predicted PEFR (P < 0.05 to 0.001). Thus women exposed to biofuels smoke suffer more from health problems and respiratory illnesses when compared with other fuel users.     

Relationships between Nitrogen Dioxide Personal Exposure and Ambient Air Monitoring Measurements among Children in Three French Metropolitan Areas: VESTA Study

In epidemiological studies, investigators have routinely used ambient air concentrations, measured by air-quality monitoring networks, to assess exposure of subjects. When there is great spatial variability of ambient air concentrations or when there are specific indoor exposures, this approach may yield substantial exposure misclassification and distort the associations between exposure and the health endpoints of interest. In 3 French metropolitan areas, the cross-sectional relationships between 48 hr of nitrogen dioxide personal exposure of 73 children and the corresponding 48-hr background ambient air concentrations were analyzed. The crude correlation between ambient air concentrations and personal exposures was poor in all cities (r ² = .009 for Grenoble, r ² = .04 for Toulouse, and r ² = .02 for Paris). These correlations were improved when the authors took into account other ambient air or indoor air sources of nitrogen dioxide emissions (the corresponding multiple linear regression, r ², increased to .43 in Grenoble, .50 in Toulouse, and .37 in Paris). The main variables that explained personal exposures were an index of traffic intensity and proximity and use of a gas cooker at home. The results of this study confirm that ambient air-monitoring site measurements are poor predictors of personal exposure. Investigators should carefully characterize the proximity of roads occupied by dense traffic to the home/school as well as indoor sources of nitric oxide emissions; both of these careful characterizations will assist researchers in the prediction of personal exposure in epidemiological studies.     

Particulate Air Pollution,Metabolic Syndrome,and Heart Rate Variability: The Multi-Ethnic Study of Atherosclerosis (MESA)

Background

Cardiac autonomic dysfunction has been suggested as a possible biologic pathway for the association between fine particulate matter ≤ 2.5 μm in diameter (PM_2.5) and cardiovascular disease (CVD). We examined the associations of PM_2.5 with heart rate variability, a marker of autonomic function, and whether metabolic syndrome (MetS) modified these associations.

Methods

We used data from the Multi-Ethnic Study of Atherosclerosis to measure the standard deviation of normal-to-normal intervals (SDNN) and the root mean square of successive differences (rMSSD) of 5,465 participants 45–84 years old who were free of CVD at the baseline examination (2000–2002). Data from the U.S. regulatory monitor network were used to estimate ambient PM_2.5 concentrations at the participants’ residences. MetS was defined as having three or more of the following criteria: abdominal obesity, hypertriglyceridemia, low high-density lipoprotein cholesterol, high blood pressure, and high fasting glucose.

Results

After controlling for confounders, we found that an interquartile range (IQR) increase in 2-day average PM_2.5 (10.2 μg/m³) was associated with a 2.1% decrease in rMSSD [95% confidence interval (CI), −4.2 to 0.0] and nonsignificantly associated with a 1.8% decrease in SDNN (95% CI, −3.7 to 0.1). Associations were stronger among individuals with MetS than among those without MetS: an IQR elevation in 2-day PM_2.5 was associated with a 6.2% decrease in rMSSD (95% CI, −9.4 to −2.9) among participants with MetS, whereas almost no change was found among participants without MetS (p-interaction = 0.005). Similar effect modification was observed in SDNN (p-interaction = 0.011).

Conclusion

These findings suggest that autonomic dysfunction may be a mechanism through which PM exposure affects cardiovascular risk, especially among persons with MetS.