Particulate matter exposures, mortality, and cardiovascular disease in the health professionals follow-up study

Background: The association of all-cause mortality and cardiovascular outcomes with air pollution exposures has been well established in the literature. The number of studies examining chronic exposures in cohorts is growing, with more recent studies conducted among women finding risk estimates of greater magnitude. Questions remain regarding sex differences in the relationship of chronic particulate matter (PM) exposures with mortality and cardiovascular outcomes.Objectives: In this study we explored these associations in the all-male Health Professionals Follow-Up Study prospective cohort.Methods: The same spatiotemporal exposure estimation models, similar outcomes, and biennially updated covariates were used as those previously applied in the female Nurses’ Health Study cohort.Results: Among 17,545 men residing in the northeastern and midwestern United States, there were 2,813 deaths, including 746 cases of fatal coronary heart disease (CHD). An interquartile range change (4 µg/m³) in average exposure to PM ≤ 2.5 µm in diameter in the 12 previous months was not associated with all-cause mortality [hazard ratio (HR) = 0.94; 95% confidence interval (CI), 0.87–1.00] or fatal CHD (HR = 0.99; 95% CI, 0.87–1.13) in fully adjusted models. Findings were similar for separate models of exposure to PM ≤ 10 µm in diameter and PM between 2.5 and 10 µm in diameter and for copollutant models.Conclusions: Among this cohort of men with high socioeconomic status living in the midwestern and northeastern United States, the results did not support an association of chronic PM exposures with all-cause mortality and cardiovascular outcomes in models with time-varying covariates. Whether these findings suggest sex differences in susceptibility or the protective impact of healthier lifestyles and higher socioeconomic status requires additional investigation.     

Indoor air pollution and blood pressure in adult women living in rural China

Background: Almost half of the world’s population uses coal and biomass fuels for domestic energy. Limited evidence suggests that exposure to air pollutants from indoor biomass combustion may be associated with elevated blood pressure (BP).Objective: Our aim was to assess the relationship between air pollution exposure from indoor biomass combustion and BP in women in rural China.Methods: We measured 24-hr personal integrated gravimetric exposure to fine particles < 2.5 µm in aerodynamic diameter (PM_2.5) and systolic BP (SBP) and diastolic BP (DBP) in the winter and summer among 280 women ≥ 25 years of age living in rural households using biomass fuels in Yunnan, China. We investigated the association between PM_2.5 exposure and SBP and DBP using mixed-effects models with random intercepts to account for correlation among repeated measures.Results: Personal average 24-hr exposure to PM_2.5 ranged from 22 to 634 µg/m³ in winter and from 9 to 492 µg/m³ in summer. A 1-log-µg/m³ increase in PM_2.5 exposure was associated with 2.2 mm Hg higher SBP [95% confidence interval (CI), 0.8 to 3.7; p = 0.003] and 0.5 mm Hg higher DBP (95% CI, –0.4 to 1.3; p = 0.31) among all women; estimated effects varied by age group. Among women > 50 years of age, a 1-log-µg/m³ increase in PM_2.5 exposure was associated with 4.1 mm Hg higher SBP (95% CI, 1.5 to 6.6; p = 0.002) and 1.8 mm Hg higher DBP (95% CI, 0.4 to 3.2; p = 0.01). PM_2.5 exposure was positively associated with SBP among younger women, but the association was not statistically significant.Conclusion: PM_2.5 exposure from biomass combustion may be a risk factor for elevated BP and hence for cardiovascular events. Our findings should be corroborated in longitudinal studies.     

Hemodynamic,Autonomic, and Vascular Effects of Exposure to Coarse Particulate Matter Air Pollution from a Rural Location

Background: Fine particulate matter (PM) air pollution is associated with numerous adverse health effects, including increased blood pressure (BP) and vascular dysfunction. Coarse PM substantially contributes to global air pollution, yet differs in characteristics from fine particles and is currently not regulated. However, the cardiovascular (CV) impacts of coarse PM exposure remain largely unknown.Objectives: Our goal was to elucidate whether coarse PM, like fine PM, is itself capable of eliciting adverse CV responses.Methods: We performed a randomized double-blind crossover study in which 32 healthy adults (25.9 ± 6.6 years of age) were exposed to concentrated ambient coarse particles (CAP; 76.2 ± 51.5 μg/m³) in a rural location and filtered air (FA) for 2 hr. We measured CV outcomes during, immediately after, and 2 hr postexposures.Results: Both systolic (mean difference = 0.32 mmHg; 95% CI: 0.05, 0.58; p = 0.021) and diastolic BP (0.27 mmHg; 95% CI: 0.003, 0.53; p = 0.05) linearly increased per 10 min of exposure during the inhalation of coarse CAP when compared with changes during FA exposure. Heart rate was on average higher (4.1 bpm; 95% CI: 3.06, 5.12; p < 0.0001) and the ratio of low-to-high frequency heart rate variability increased (0.24; 95% CI: 0.07, 0.41; p = 0.007) during coarse particle versus FA exposure. Other outcomes (brachial flow-mediated dilatation, microvascular reactive hyperemia index, aortic hemodynamics, pulse wave velocity) were not differentially altered by the exposures.Conclusions: Inhalation of coarse PM from a rural location is associated with a rapid elevation in BP and heart rate during exposure, likely due to the triggering of autonomic imbalance. These findings add mechanistic evidence supporting the biological plausibility that coarse particles could contribute to the triggering of acute CV events.Citation: Brook RD, Bard RL, Morishita M, Dvonch JT, Wang L, Yang HY, Spino C, Mukherjee B, Kaplan MJ, Yalavarthi S, Oral EA, Ajluni N, Sun Q, Brook JR, Harkema J, Rajagopalan S. 2014. Hemodynamic, autonomic, and vascular effects of exposure to coarse particulate matter air pollution from a rural location. Environ Health Perspect 122:624–630; http://dx.doi.org/10.1289/ehp.1306595     

In-traffic air pollution exposure and CC16, blood coagulation, and inflammation markers in healthy adults

Background: Exposure to traffic-related air pollution is a risk factor for cardiovascular events, probably involving mechanisms of inflammation and coagulation. Little is known about effects of the short exposures encountered while participating in traffic.Objectives: The objective of the study was to examine effects of exposure of commuters to air pollution on cardiovascular biomarkers.Methods: Thirty-four healthy adult volunteers commuted for 2 hr by bus, car, or bicycle during the morning rush hour. During the commute, exposure to particle number, particulate matter (PM) ≤ 2.5 µm in aerodynamic diameter (PM_2.5), PM ≤ 10 µm in diameter (PM₁₀), and soot was measured. We estimated inhaled doses based on heart rate monitoring. Shortly before exposure and 6 hr after exposure, blood samples were taken and analyzed for CC16 (Clara cell protein 16), blood cell count, coagulation markers, and inflammation markers. Between June 2007 and June 2008, 352 pre- and postexposure blood samples were collected on 47 test days. We used mixed models to analyze the associations between exposure and changes in health parameters.Results: We observed no consistent associations between the air pollution exposures and doses and the various biomarkers that we investigated.Conclusions: Air pollution exposure during commuting was not consistently associated with acute changes in inflammation markers, blood cell counts, or blood coagulation markers.     

Intervention to lower household wood smoke exposure in Guatemala reduces ST-segment depression on electrocardiograms

Background: A large body of evidence suggests that fine particulate matter (PM) air pollution is a cause of cardiovascular disease, but little is known in particular about the cardiovascular effects of indoor air pollution from household use of solid fuels in developing countries. RESPIRE (Randomized Exposure Study of Pollution Indoors and Respiratory Effects) was a randomized trial of a chimney woodstove that reduces wood smoke exposure.Objectives: We tested the hypotheses that the stove intervention, compared with open fire use, would reduce ST-segment depression and increase heart rate variability (HRV).Methods: We used two complementary study designs: a) between-groups comparisons based on randomized stove assignment, and b) before-and-after comparisons within control subjects who used open fires during the trial and received chimney stoves after the trial. Electrocardiogram sessions that lasted 20 hr were repeated up to three times among 49 intervention and 70 control women 38–84 years of age, and 55 control subjects were also assessed after receiving stoves. HRV and ST-segment values were assessed for each 30-min period. ST-segment depression was defined as an average value below –1.00 mm. Personal fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] exposures were measured for 24 hr before each electrocardiogram.Results: PM_2.5 exposure means were 266 and 102 μg/m³ during the trial period in the control and intervention groups, respectively. During the trial, the stove intervention was associated with an odds ratio of 0.26 (95% confidence interval, 0.08–0.90) for ST-segment depression. We found similar associations with the before-and-after comparison. The intervention was not significantly associated with HRV.Conclusions: The stove intervention was associated with reduced occurrence of nonspecific ST-segment depression, suggesting that household wood smoke exposures affect ventricular repolarization and potentially cardiovascular health.     

Retinal Microvascular Responses to Short-Term Changes in Particulate Air Pollution in Healthy Adults

Background: Microcirculation plays an important role in the physiology of cardiovascular health. Air pollution is an independent risk factor for the development and progression of cardiovascular diseases, but the number of studies on the relation between air pollution and the microcirculation is limited.Objectives: We examined the relationship between short-term changes in air pollution and microvascular changes.Methods: We measured retinal microvasculature using fundus image analysis in a panel of 84 healthy adults (52% female), 22–63 years of age, during January–May 2012. Blood vessels were measured as central retinal arteriolar/venular equivalent (CRAE/CRVE), with a median of 2 measurements (range, 1–3). We used monitoring data on particulate air pollution (PM₁₀) and black carbon (BC). Mixed-effect models were used to estimate associations between CRAE/CRVE and exposure to PM₁₀ and BC using various exposure windows.Results: CRAE and CRVE were associated with PM₁₀ and BC concentrations, averaged over the 24 hr before the retinal examinations. Each 10-µg/m³ increase in PM₁₀ was associated with a 0.93-µm decrease (95% CI: –1.42, –0.45; p = 0.0003) in CRAE and a 0.86-µm decrease (95% CI: –1.42, –0.30; p = 0.004) in CRVE after adjusting for individual characteristics and time varying conditions such as ambient temperature. Each 1-µg/m³ increase in BC was associated with a 1.84-µm decrease (95% CI: –3.18, –0.51; p < 0.001) in CRAE.Conclusions: Our findings suggest that the retinal microvasculature responds to short-term changes in air pollution levels. These results support a mechanistic pathway through which air pollution can act as a trigger of cardiovascular events at least in part through effects on the microvasculature.Citation: Louwies T, Int Panis L, Kicinski M, De Boever P, Nawrot TS. 2013. Retinal microvascular responses to short-term changes in particulate air pollution in healthy adults. Environ Health Perspect 121:1011–1016; http://dx.doi.org/10.1289/ehp.1205721     

Ambient air pollution and lipoprotein-associated phospholipase A₂ in survivors of myocardial infarction

Background: Increasing evidence suggests a proatherogenic role for lipoprotein-associated phospholipase A₂ (Lp-PLA2). A meta-analysis of published cohorts has shown that Lp-PLA2 is an independent predictor of coronary heart disease events and stroke.Objective: In this study, we investigated whether the association between air pollution and cardiovascular disease might be partly explained by increased Lp-PLA2 mass in response to exposure.Methods: A prospective longitudinal study of 200 patients who had had a myocardial infarction was performed in Augsburg, Germany. Up to six repeated clinical examinations were scheduled every 4–6 weeks between May 2003 and March 2004. Supplementary to the multicenter AIRGENE protocol, we assessed repeated plasma Lp-PLA2 concentrations. Air pollution data from a fixed monitoring site representing urban background concentrations were collected. We measured hourly means of particle mass [particulate matter (PM) < 10 µm (PM₁₀) and PM < 2.5 µm (PM_2.5) in aerodynamic diameter] and particle number concentrations (PNCs), as well as the gaseous air pollutants carbon monoxide (CO), sulfur dioxide (SO₂), ozone (O₃), nitric oxide (NO), and nitrogen dioxide (NO₂). Data were analyzed using mixed models with random patient effects.Results: Lp-PLA2 showed a positive association with PM₁₀, PM_2.5, and PNCs, as well as with CO, NO₂, NO, and SO₂ 4–5 days before blood withdrawal (lag 4–5). A positive association with O₃ was much more immediate (lag 0). However, inverse associations with some pollutants were evident at shorter time lags.Conclusion: These preliminary findings should be replicated in other study populations because they suggest that the accumulation of acute and subacute effects or the chronic exposure to ambient particulate and gaseous air pollution may result in the promotion of atherosclerosis, mediated, at least in part, by increased levels of Lp-PLA2.     

Does Air Pollution Trigger Infant Mortality in Western Europe? A Case-Crossover Study

Background: Numerous studies show associations between fine particulate air pollutants [particulate matter with an aerodynamic diameter ≤ 10 μm (PM₁₀)] and mortality in adults.Objectives: We investigated short-term effects of elevated PM₁₀ levels on infant mortality in Flanders, Belgium, and studied whether the European Union (EU) limit value protects infants from the air pollution trigger.Methods: In a case-crossover analysis, we estimated the risk of dying from nontraumatic causes before 1 year of age in relation to outdoor PM₁₀ concentrations on the day of death. We matched control days on temperature to exclude confounding by variations in daily temperature.Results: During the study period (1998–2006), PM₁₀ concentration averaged 31.9 ± 13.8 μg/m³. In the entire study population (n = 2,382), the risk of death increased by 4% [95% confidence interval (CI), 0–8%; p = 0.045] for a 10-μg/m³ increase in daily mean PM₁₀. However, this association was significant only for late neonates (2–4 weeks of age; n = 372), in whom the risk of death increased by 11% (95% CI, 1–22%; p = 0.028) per 10-μg/m³ increase in PM₁₀. In this age class, infants were 1.74 (95% CI, 1.18–2.58; p = 0.006) times more likely to die on days with a mean PM₁₀ above the EU limit value of 50 μg/m³ than on days below this cutoff.Conclusions: Even in an affluent region in Western Europe, where infant mortality is low, days with higher PM air pollution are associated with an increased risk of infant mortality. Assuming causality, the current EU limit value for PM₁₀, which may be exceeded on 35 days/year, does not prevent PM₁₀ from triggering mortality in late neonates.     

The effects of particulate matter sources on daily mortality: a case-crossover study of Barcelona, Spain

Background: Dozens of studies link acute exposure to particulate matter (PM) air pollution with premature mortality and morbidity, but questions remain about which species and sources in the vast PM mixture are responsible for the observed health effects. Although a few studies exist on the effects of species and sources in U.S. cities, European cities—which have a higher proportion of diesel engines and denser urban populations—have not been well characterized. Information on the effects of specific sources could aid in targeting pollution control and in articulating the biological mechanisms of PM.Objectives: Our study examined the effects of various PM sources on daily mortality for 2003 through 2007 in Barcelona, a densely populated city in the northeast corner of Spain.Methods: Source apportionment for PM ≤ 2.5 μm and ≤ 10 µm in aerodynamic diameter (PM_2.5 and PM₁₀) using positive matrix factorization identified eight different factors. Case-crossover regression analysis was used to estimate the effects of each factor.Results: Several sources of PM_2.5, including vehicle exhaust, fuel oil combustion, secondary nitrate/organics, minerals, secondary sulfate/organics, and road dust, had statistically significant associations (p < 0.05) with all-cause and cardiovascular mortality. Also, in some cases relative risks for a respective interquartile range increase in concentration were higher for specific sources than for total PM_2.5 mass.Conclusions: These results along with those from our multisource models suggest that traffic, sulfate from shipping and long-range transport, and construction dust are important contributors to the adverse health effects linked to PM.     

Long-term exposure to traffic-related air pollution and the risk of coronary heart disease hospitalization and mortality

Background

Epidemiologic studies have demonstrated that exposure to road traffic is associated with adverse cardiovascular outcomes.

Objectives

We aimed to identify specific traffic-related air pollutants that are associated with the risk of coronary heart disease (CHD) morbidity and mortality to support evidence-based environmental policy making.

Methods

This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents 45–85 years of age who resided in Metropolitan Vancouver during the exposure period and without known CHD at baseline were included in this study (n = 452,735). Individual exposures to traffic-related air pollutants including black carbon, fine particles [aerodynamic diameter ≤ 2.5 μm (PM_2.5)], nitrogen dioxide (NO₂), and nitric oxide were estimated at residences of the subjects using land-use regression models and integrating changes in residences during the exposure period. CHD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration records.

Results

An interquartile range elevation in the average concentration of black carbon (0.94 × 10⁻⁵/m filter absorbance, equivalent to approximately 0.8 μg/m³ elemental carbon) was associated with a 3% increase in CHD hospitalization (95% confidence interval, 1–5%) and a 6% increase in CHD mortality (3–9%) after adjusting for age, sex, preexisting comorbidity, neighborhood socioeconomic status, and copollutants (PM_2.5 and NO₂). There were clear linear exposure–response relationships between black carbon and coronary events.

Conclusions

Long-term exposure to traffic-related fine particulate air pollution, indicated by black carbon, may partly explain the observed associations between exposure to road traffic and adverse cardiovascular outcomes.     

Acute effects of fine particulate air pollution on cardiac arrhythmia: the APACR study

Background: The mechanisms underlying the relationship between particulate matter (PM) air pollution and cardiac disease are not fully understood.Objectives: We examined the effects and time course of exposure to fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] on cardiac arrhythmia in 105 middle-age community-dwelling healthy nonsmokers in central Pennsylvania.Methods: The 24-hr beat-to-beat electrocardiography data were obtained using a high-resolution Holter system. After visually identifying and removing artifacts, we summarized the total number of premature ventricular contractions (PVCs) and premature atrial contractions (PACs) for each 30-min segment. A personal PM_2.5 nephelometer was used to measure individual-level real-time PM_2.5 exposures for 24 hr. We averaged these data to obtain 30-min average time–specific PM_2.5 exposures. Distributed lag models under the framework of negative binomial regression and generalized estimating equations were used to estimate the rate ratio between 10-μg/m³ increases in average PM_2.5 over 30-min intervals and ectopy counts.Results: The mean ± SD age of participants was 56 ± 8 years, with 40% male and 73% non-Hispanic white. The 30-min mean ± SD for PM_2.5 exposure was 13 ± 22 μg/m³, and PAC and PVC counts were 0.92 ± 4.94 and 1.22 ± 7.18. Increases of 10 μg/m³ in average PM_2.5 concentrations during the same 30 min or the previous 30 min were associated with 8% and 3% increases in average PVC counts, respectively. PM_2.5 was not significantly associated with PAC count.Conclusion: PM_2.5 exposure within approximately 60 min was associated with increased PVC counts in healthy individuals.     

Omega-3 fatty acid supplementation appears to attenuate particulate air pollution-induced cardiac effects and lipid changes in healthy middle-aged adults

Background: Air pollution exposure has been associated with adverse cardiovascular health effects. Findings of a recent epidemiological study suggested that omega-3 fatty acid (fish oil) supplementation blunted cardiac responses to air pollution exposure.Objectives: We conducted a randomized, controlled exposure study to evaluate the efficacy of fish oil supplements in attenuating adverse cardiac effects of exposure to concentrated ambient fine and ultrafine particulate matter (CAP).Methods: Twenty-nine healthy middle-aged participants (mean, 58 ± 1 years of age) were supplemented in a randomized, double-blinded manner with 3 g/day of either fish oil or olive oil for 4 weeks before sequential chamber exposure to filtered air and CAP (mean mass concentration 278 ± 19 µg/m³) for 2 hr. Cardiac responses were assessed by comparing time and frequency domain changes in heart rate variability (HRV) and electrocardiographic repolarization changes measured before, immediately after, and 20 hr after exposure. Changes in plasma lipids were also evaluated at these time points.Results: Fish oil supplementation appeared to attenuate CAP-induced reductions in high-frequency/low-frequency ratio, as well as elevations in normalized low-frequency HRV and prolongation of the QT interval corrected for heart rate (QTc). Very low-density lipoprotein and triglyceride concentrations increased significantly immediately after exposure to CAP in participants supplemented with olive oil, but not in those supplemented with fish oil.Conclusions: Exposure of healthy middle-aged adults to CAP for 2 hr induced acute cardiac and lipid changes after supplementation with olive oil, but not fish oil. Our findings suggest that omega-3 fatty acid supplements offer protection against the adverse cardiac and lipid effects associated with air pollution exposure.     

Effect of Cheese Intake on Cardiovascular Diseases and Cardiovascular Biomarkers

Background: A growing number of cohort studies revealed an inverse association between cheese intake and cardiovascular diseases, yet the causal relationship is unclear. Objective: To assess the causal relationship between cheese intake, and cardiovascular diseases and cardiovascular biomarkers. Methods: A two-sample Mendelian randomization (MR) analysis based on publicly available genome-wide association studies was employed to infer the causal relationship. The effect estimates were calculated using the random-effects inverse-variance-weighted method. Results: Cheese intake per standard deviation increase causally reduced the risks of type 2 diabetes (odds ratio (OR) = 0.46; 95% confidence interval (CI), 0.34–0.63; p = 1.02 × 10⁻⁶), heart failure (OR = 0.62; 95% CI, 0.49–0.79; p = 0.0001), coronary heart disease (OR = 0.65; 95% CI, 0.53–0.79; p = 2.01 × 10⁻⁵), hypertension (OR = 0.67; 95% CI, 0.53–0.84; p = 0.001), and ischemic stroke (OR = 0.76; 95% CI, 0.63–0.91; p = 0.003). Suggestive evidence of an inverse association between cheese intake and peripheral artery disease was also observed. No associations were observed for atrial fibrillation, cardiac death, pulmonary embolism, or transient ischemic attack. The better prognosis associated with cheese intake may be explained by lower body mass index (BMI; effect estimate = −0.58; 95% CI, from −0.88 to −0.27; p = 0.0002), waist circumference (effect estimate = −0.49; 95% CI, from −0.76 to −0.23; p = 0.0003), triglycerides (effect estimate = −0.33; 95% CI, from −0.50 to −0.17; p = 4.91 × 10⁻⁵), and fasting glucose (effect estimate = −0.20; 95% CI, from −0.33 to −0.07; p = 0.0003). There was suggestive evidence of a positive association between cheese intake and high-density lipoprotein. No influences were observed for blood pressure or inflammation biomarkers. Conclusions: This two-sample MR analysis found causally inverse associations between cheese intake and type 2 diabetes, heart failure, coronary heart disease, hypertension, and ischemic stroke.     

Residential exposure to outdoor air pollution during pregnancy and anthropometric measures at birth in a multicenter cohort in Spain

Background: A growing body of research suggests that prenatal exposure to air pollution may be harmful to fetal development. We assessed the association between exposure to air pollution during pregnancy and anthropometric measures at birth in four areas within the Spanish Children’s Health and Environment (INMA) mother and child cohort study.Methods: Exposure to ambient nitrogen dioxide (NO₂) and benzene was estimated for the residence of each woman (n = 2,337) for each trimester and for the entire pregnancy. Outcomes included birth weight, length, and head circumference. The association between residential outdoor air pollution exposure and birth outcomes was assessed with linear regression models controlled for potential confounders. We also performed sensitivity analyses for the subset of women who spent more time at home during pregnancy. Finally, we performed a combined analysis with meta-analysis techniques.Results: In the combined analysis, an increase of 10 µg/m³ in NO₂ exposure during pregnancy was associated with a decrease in birth length of –0.9 mm [95% confidence interval (CI), –1.8 to –0.1 mm]. For the subset of women who spent ≥ 15 hr/day at home, the association was stronger (–0.16 mm; 95% CI, –0.27 to –0.04). For this same subset of women, a reduction of 22 g in birth weight was associated with each 10-µg/m³ increase in NO₂ exposure in the second trimester (95% CI, –45.3 to 1.9). We observed no significant relationship between benzene levels and birth outcomes.Conclusions: NO₂ exposure was associated with reductions in both length and weight at birth. This association was clearer for the subset of women who spent more time at home.     

Assessing the influence of indoor exposure to "outdoor ozone" on the relationship between ozone and short-term mortality in U.S. communities

Background: City-to-city differences have been reported for the increase in short-term mortality associated with a given increase in ozone concentration (ozone mortality coefficient). Although ozone concentrations are monitored at central outdoor locations, a large fraction of total ozone exposure occurs indoors.Objectives: To clarify the influence of indoor exposure to ozone of outdoor origin on short-term mortality, we conducted an analysis to determine whether variation in ozone mortality coefficients among U.S. cities might be partly explained by differences in total ozone exposure (from both outdoor and indoor exposures) resulting from the same outdoor ozone concentration.Methods: We estimated average annual air change rates (the overall rate at which indoor air is replaced with outdoor air) and used these to estimate the change in total ozone exposure per unit change in outdoor ozone exposure (ozone exposure coefficient) for 18 cities that had been included in the National Morbidity and Mortality Air Pollution Study (NMMAPS). We then examined associations between both parameters and published ozone mortality coefficients.Results: For the 18 targeted NMMAPS cities, the association between ozone mortality coefficients and ozone exposure coefficients was strong (1-hr ozone metric: R² = 0.58, p < 0.001; 8-hr ozone: R² = 0.56, p < 0.001; 24-hr ozone: R² = 0.48, p = 0.001). When extended to another 72 NMMAPS cities, the associations remained strong (R² = 0.47–0.63; p < 0.001).Conclusions: Differences in ozone mortality coefficients among cities appear to partially reflect differences in total ozone exposure resulting from differences in the amount of outdoor ozone that is transported indoors.     

Controlled Exposures to Air Pollutants and Risk of Cardiac Arrhythmia

Background: Epidemiological studies have reported associations between air pollution exposure and increases in cardiovascular morbidity and mortality. Exposure to air pollutants can influence cardiac autonomic tone and reduce heart rate variability, and may increase the risk of cardiac arrhythmias, particularly in susceptible patient groups.Objectives: We investigated the incidence of cardiac arrhythmias during and after controlled exposure to air pollutants in healthy volunteers and patients with coronary heart disease.Methods: We analyzed data from 13 double-blind randomized crossover studies including 282 participants (140 healthy volunteers and 142 patients with stable coronary heart disease) from whom continuous electrocardiograms were available. The incidence of cardiac arrhythmias was recorded for each exposure and study population.Results: There were no increases in any cardiac arrhythmia during or after exposure to dilute diesel exhaust, wood smoke, ozone, concentrated ambient particles, engineered carbon nanoparticles, or high ambient levels of air pollution in either healthy volunteers or patients with coronary heart disease.Conclusions: Acute controlled exposure to air pollutants did not increase the short-term risk of arrhythmia in participants. Research employing these techniques remains crucial in identifying the important pathophysiological pathways involved in the adverse effects of air pollution, and is vital to inform environmental and public health policy decisions.Citation: Langrish JP, Watts SJ, Hunter AJ, Shah AS, Bosson JA, Unosson J, Barath S, Lundbäck M, Cassee FR, Donaldson K, Sandström T, Blomberg A, Newby DE, Mills NL. 2014. Controlled exposures to air pollutants and risk of cardiac arrhythmia. Environ Health Perspect 122:747–753; http://dx.doi.org/10.1289/ehp.1307337     

Adverse Health Effects of Child Labor: High Exposure to Chromium and Oxidative DNA Damage in Children Manufacturing Surgical Instruments

Background: A considerable part of the worldwide production of surgical instruments takes place in Sialkot, Pakistan. Many children work in hazardous conditions in this industry.Objective: We investigated exposure to metals and possible health effects among children working in surgical instruments manufacturing units compared with schoolchildren from the same city.Methods: In a cross-sectional study we studied a convenience sample of 104 male children (10–14 years of age) working in surgical instruments manufacturing units and 75 male children of similar age from a school in Sialkot, Pakistan. A respiratory questionnaire was administered, spirometry was performed, and blood pressure was measured. In a spot urine sample, concentrations of metals were measured by inductively coupled plasma mass spectrometry and 8-hydroxydeoxyguanosine (8OHdG, reflecting oxidative DNA damage) by ELISA.Results: The working children reported more asthma (10% vs. 0%; p = 0.005) and dry cough at night (36% vs. 20%; p = 0.02) than did the schoolchildren, but there were no significant differences in pulmonary function or blood pressure. The urinary concentration of chromium was 35 times higher in working children [geometric mean, 23.0 µg/L; 25th–75th percentile, 8.38–58.6] than in schoolchildren [0.66 µg/L; 0.38–1.09)], and largely in excess of the occupational Biological Exposure Index for adult workers (25 µg/L). Urinary 8-OHdG concentrations were not significantly higher in working children than in schoolchildren (19.3 vs. 17.6 µg/g creatinine, p = 0.4), but were significantly correlated with urinary nickel (r = 0.41; p < 0.0001) and with a composite index of metal exposure (r = 0.46; p < 0.0001).Conclusions: Children working in the surgical instruments manufacturing industry had substantial exposure to several metals, especially chromium and nickel, which are established carcinogens. Exposure to nickel was associated with evidence of increased oxidative DNA damage.     

Long Chain Omega-3 Polyunsaturated Fatty Acids Improve Vascular Stiffness in Abdominal Aortic Aneurysm: A Randomized Controlled Trial

Abdominal aortic aneurysm (AAA) is a vascular disease involving permanent focal dilation of the abdominal aorta (≥30 mm) that can lead to catastrophic rupture. Destructive remodeling of aortic connective tissue in AAA contributes to wall stiffening, a mechanical parameter of the arterial system linked to a heightened risk of cardiovascular morbidity and mortality. Since aortic stiffening is associated with AAA progression, treatment options that target vascular inflammation would appear prudent. Given this, and growing evidence indicating robust anti-inflammatory and vasoprotective properties for long chain omega-3 polyunsaturated fatty acids (LC n-3 PUFAs), this study evaluated the impact of these nutrients (1.8 g/day for 12 weeks) on indices of vascular stiffness in patients with AAA. At baseline, pulse wave velocity (PWV) and augmentation index normalized to a heart rate of 75 bpm (AIx75) were significantly higher in patients with AAA compared to control participants (PWV: 14.2 ± 0.4 m.s⁻¹ vs. 12.6 ± 0.4 m.s⁻¹, p = 0.014; AIx75: 26.4 ± 1.7% vs. 17.3 ± 2.7%, p = 0.005). Twelve-week LC n-3 PUFA supplementation significantly decreased PWV (baseline: 14.2 ± 0.6 m.s⁻¹, week 12: 12.8 ± 0.7 m.s⁻¹, p = 0.014) and heart rate (baseline: 63 ± 3 bpm, week 12: 58 ± 3 bpm, p = 0.009) in patients with AAA. No change was observed for patients receiving placebo capsules. While this raises the possibility that LC n-3 PUFAs provide improvements in aortic stiffness in patients with AAA, the clinical implications remain to be fully elucidated.     

Ambient Air Pollution and Adult Asthma Incidence in Six European Cohorts (ESCAPE)

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 PM_coarse. 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), PM_2.5 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 5 μg/m³), PM_{2.5absorbance} (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 PM_coarse (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