Long-term ambient multipollutant exposures and mortality.
ABSTRACT: population-based studies have demonstrated associations between ambient air pollution exposures and mortality, but few have been able to adjust for occupational exposures. Additionally, two studies have observed higher risks in individuals with occupational dust, gas, or fume exposure.we examined the association of ambient residential exposure to particulate matter less than 10 microm in diameter (PM(10)), particulate matter less than 2.5 microm in diameter (PM(2.5)), NO(2), SO(2), and mortality in 53,814 men in the U.S. trucking industry.exposures for PM(10), NO(2), and SO(2) at each residential address were assigned using models combining spatial smoothing and geographic covariates. PM(2.5) exposures in 2000 were assigned from the nearest available monitor. Single and multipollutant Cox proportional hazard models were used to examine the association of an interquartile range (IQR) change (6 microg/m(3) for PM(10), 4 microg/m(3) for PM(2.5), 4ppb for SO(2), and 8ppb for NO(2)) and the risk of all-cause and cause-specific mortality.an IQR change in ambient residential exposures to PM(10) was associated with a 4.3% (95% confidence interval [CI], 1.1-7.7%) increased risk of all-cause mortality. The increase for an IQR change in SO(2) was 6.9% (95% CI, 2.3-11.6%), for NO(2) was 8.2% (95% CI, 4.5-12.1%), and for PM(2.5) was 3.9% (95% CI, 1.0-6.9%). Elevated associations with cause-specific mortality (lung cancer, cardiovascular and respiratory disease) were observed for PM(2.5), SO(2), and NO(2), but not PM(10). None of the pollutants were confounded by occupational exposures. In multipollutant models, overall, the associations were attenuated, most strongly for PM(10). In sensitivity analyses excluding long-haul drivers, who spend days away from home, larger hazard ratios were observed.in this population of men, residential ambient air pollution exposures were associated with mortality.
Project description:Background: Direct and continuous exposure to particulate matter (PM), especially in occupational settings is known to impact negatively on respiratory health and lung function. Objective: To determine the association between concentrations of PM (2.5, 2.5-10 and 10 µm) in breathing zone and lung function of informal e-waste workers at Agbogbloshie. Methods: To evaluate lung function responses to PM (2.5, 2.5-10 and 10 µm), we conducted a longitudinal cohort study with three repeated measures among 207 participants comprising 142 healthy e-waste workers from Agbogbloshie scrapyard and 65 control participants from Madina-Zongo in Accra, Ghana from 2017-2018. Lung function parameters (FVC, FEV1, FEV1/FVC, PEF, and FEF 25-75) and PM (2.5, 2.5-10 and 10 µm) concentrations were measured, corresponding to prevailing seasonal variations. Socio-demographic data, respiratory exposures and lifestyle habits were determined using questionnaires. Random effects models were then used to examine the effects of PM (2.5, 2.5-10 and 10 µm) on lung function. Results: The median concentrations of PM (2.5, 2.5-10 and 10 µm) were all consistently above the WHO ambient air standards across the study waves. Small effect estimates per IQR of PM (2.5, 2.5-10 and 10 µm) on lung function parameters were observed even after adjustment for potential confounders. However, a 10 µg increase in PM (2.5, 2.5-10 and 10 µm) was associated with decreases in PEF and FEF 25-75 by 13.3% % [? = -3.133; 95% CI: -0.243, -0.022) and 26.6% [? = -0.266; 95% CI: -0.437, 0.094]. E-waste burning and a history of asthma significantly predicted a decrease in PEF by 14.2% [? = -0.142; 95% CI: -0.278, -0.008) and FEV1 by 35.8% [? = -0.358; 95% CI: -0.590, 0.125] among e-waste burners. Conclusions: Direct exposure of e-waste workers to PM predisposes to decline in lung function and risk for small airway diseases such as asthma and COPD.
Project description:Central monitoring site (CMS) concentrations have been used to represent population-based personal exposures to particulate matter (PM) of ambient origin. We investigated the associations of the concentrations of PM(2.5) and PM(10) and their elemental components for elderly clinic patients with chronic obstructive pulmonary disease in two cities with different PM compositions, that is, New York City (NYC) and Seattle. Daily measurements of CMS, outdoor residential, and indoor PM(10) and PM(2.5) concentrations, as well as personal PM(10), were made concurrently for 12-consecutive winter days at 9 NYC and 15 Seattle residences, as well for 9 NYC residences in summer. Filters were analyzed for elemental components using X-ray fluorescence (XRF), and for black carbon (BC) by light reflectance, and outdoor-indoor-personal relationships of PM components were examined using mixed-effect models. Using sulfur (S) as a tracer of PM of ambient origin, the mean contributions of outdoor PM(2.5) was 55.2% of the indoor concentrations in NYC, and 80.0% in Seattle, and outdoor PM(2.5) in NYC and Seattle were 19.7 and 18.5% of personal PM(2.5) concentration. S was distributed homogeneously in both cities (R(2)=0.65), whereas nickel (R(2)=0.23) was much more spatially heterogeneous. Thus, CMS measurements can adequately reflect personal exposures for spatially uniform components, such as sulfate, but they are not adequate for components from more local sources.
Project description:BACKGROUND:Environmental factors may contribute to the development of Kawasaki disease in children, but prenatal environmental exposures are understudied. OBJECTIVE:We used a population-based cohort to investigate whether prenatal exposure to outdoor air pollution is associated with the incidence of Kawasaki disease in childhood. METHODS:We performed a longitudinal cohort study of all children born in Quebec, Canada, between 2006 and 2012. Children were followed for Kawasaki disease from birth until 31 March 2018. We assigned prenatal air pollutant exposure according to the residential postal code at birth. The main exposure was annual average concentration of ambient fine particulate matter [PM ?2.5?m in aerodynamic diameter (PM2.5) and nitrogen dioxide (NO2) from satellite-based estimates and land-use regression models. As secondary exposures, we considered industrial PM2.5, NO2, and sulfur dioxide (SO2) emissions estimated from dispersion models. We estimated hazard ratios (HRs) using Cox proportional hazards models, adjusted for maternal age, parity, sex, multiple birth, maternal smoking during pregnancy, socioeconomic status, birth year, and rural residence. We considered single and multipollutant models. We performed several sensitivity analyses, including assessing modifying effects of maternal comorbidities (e.g., diabetes, preeclampsia). RESULTS:The cohort comprised 505,336 children, including 539 with Kawasaki disease. HRs for each interquartile range increase in ambient air pollution were 1.16 (95% CI: 0.96, 1.39) for PM2.5 and 1.12 (95% CI: 0.96, 1.31) for NO2. For industrial air pollution, HRs were 1.07 (95% CI: 1.01, 1.13) for SO2, 1.09 (95% CI: 0.99, 1.20) for NO2, and 1.01 (95% CI: 0.97, 1.05) for PM2.5. In multipollutant models, associations for ambient PM2.5 and NO2 (i.e., from all sources) were robust to adjustment for industrial pollution, and vice versa. DISCUSSION:In this population-based cohort study, both prenatal exposure to ambient and industrial air pollution were associated with the incidence of Kawasaki disease in childhood. Further studies are needed to consolidate the observed associations. https://doi.org/10.1289/EHP6920.
Project description:Using a case-crossover study design and conditional logistic regression, we compared the relative odds of transmural (full-wall) myocardial infarction (MI) calculated using exposure surrogates that account for human activity patterns and the indoor transport of ambient PM(2.5) with those calculated using central-site PM(2.5) concentrations to estimate exposure to PM(2.5) of outdoor origin (exposure to ambient PM(2.5)). Because variability in human activity and indoor PM(2.5) transport contributes exposure error in epidemiologic analyses when central-site concentrations are used as exposure surrogates, we refer to surrogates that account for this variability as "refined" surrogates. As an alternative analysis, we evaluated whether the relative odds of transmural MI associated with increases in ambient PM(2.5) is modified by residential air exchange rate (AER), a variable that influences the fraction of ambient PM(2.5) that penetrates and persists indoors. Use of refined exposure surrogates did not result in larger health effect estimates (ORs=1.10-1.11 with each interquartile range (IQR) increase), narrower confidence intervals, or better model fits compared with the analysis that used central-site PM(2.5). We did observe evidence for heterogeneity in the relative odds of transmural MI with residential AER (effect-modification), with residents of homes with higher AERs having larger ORs than homes in lower AER tertiles. For the level of exposure-estimate refinement considered here, our findings add support to the use of central-site PM(2.5) concentrations for epidemiological studies that use similar case-crossover study designs. In such designs, each subject serves as his or her own matched control. Thus, exposure error related to factors that vary spatially or across subjects should only minimally impact effect estimates. These findings also illustrate that variability in factors that influence the fraction of ambient PM(2.5) in indoor air (e.g., AER) could possibly bias health effect estimates in study designs for which a spatiotemporal comparison of exposure effects across subjects is conducted.
Project description:BACKGROUND:Long-term exposure to particulate matter (PM) in ambient air has been associated with cardiovascular mortality, but few studies have considered incident disease in relation to PM from different sources. OBJECTIVES:We aimed to study associations between long-term exposure to different types of PM and sources, and incident ischemic heart disease (IHD) and stroke in three Swedish cities. METHODS:Based on detailed emission databases, monitoring data, and high-resolution dispersion models, we calculated source contributions to PM with aerodynamic diameter ?10?m (PM10), PM with aerodynamic diameter ?2.5?m (PM2.5), and black carbon (BC) from road wear, traffic exhaust, residential heating, and other sources in Gothenburg, Stockholm, and Umeå. Registry data for participants from four cohorts were used to obtain incidence of IHD and stroke for first hospitalization or death. We constructed time windows of exposure for same-year, 1- to 5-y, and 6- to 10-y averages preceding incidence from annual averages at residential addresses. Risk estimates were based on random effects meta-analyses of cohort-specific Cox proportional hazard models. RESULTS:We observed 5,166 and 3,119 incident IHD and stroke cases, respectively, in 114,758 participants. Overall, few consistent associations were observed between the different air pollution measures and IHD or stroke incidence. However, same-year levels of ambient locally emitted BC (range: 0.01-4.6??g/m3) were associated with a 4.0% higher risk of incident stroke per interquartile range (IQR), 0.30??g/m3 [95% confidence interval (CI): 0.04, 7.8]. This association was primarily related to BC from traffic exhaust. PM10 (range: 4.4-52??g/m3) and PM2.5 (range: 2.9-22??g/m3) were not associated with stroke. Associations with incident IHD were observed only for PM2.5 exposure from residential heating. DISCUSSION:Few consistent associations were observed between different particulate components and IHD or stroke. However, long-term residential exposure to locally emitted BC from traffic exhaust was associated with stroke incidence. The comparatively low exposure levels may have contributed to the paucity of associations. https://doi.org/10.1289/EHP4757.
Project description:Previous studies reported adverse impacts of traffic-related air pollution exposure on pregnancy outcomes. Yet, little information exists on how effect estimates are impacted by the different exposure assessment methods employed in these studies.To compare effect estimates for traffic-related air pollution exposure and preeclampsia, preterm birth (gestational age less than 37 weeks), and very preterm birth (gestational age less than 30 weeks) based on four commonly used exposure assessment methods.We identified 81,186 singleton births during 1997-2006 at four hospitals in Los Angeles and Orange Counties, California. Exposures were assigned to individual subjects based on residential address at delivery using the nearest ambient monitoring station data [carbon monoxide (CO), nitrogen dioxide (NO(2)), nitric oxide (NO), nitrogen oxides (NO(x)), ozone (O(3)), and particulate matter less than 2.5 (PM(2.5)) or less than 10 (PM(10))?m in aerodynamic diameter], both unadjusted and temporally adjusted land-use regression (LUR) model estimates (NO, NO(2), and NO(x)), CALINE4 line-source air dispersion model estimates (NO(x) and PM(2.5)), and a simple traffic-density measure. We employed unconditional logistic regression to analyze preeclampsia in our birth cohort, while for gestational age-matched risk sets with preterm and very preterm birth we employed conditional logistic regression.We observed elevated risks for preeclampsia, preterm birth, and very preterm birth from maternal exposures to traffic air pollutants measured at ambient stations (CO, NO, NO(2), and NO(x)) and modeled through CALINE4 (NO(x) and PM(2.5)) and LUR (NO(2) and NO(x)). Increased risk of preterm birth and very preterm birth were also positively associated with PM(10) and PM(2.5) air pollution measured at ambient stations. For LUR-modeled NO(2) and NO(x) exposures, elevated risks for all the outcomes were observed in Los Angeles only--the region for which the LUR models were initially developed. Unadjusted LUR models often produced odds ratios somewhat larger in size than temporally adjusted models. The size of effect estimates was smaller for exposures based on simpler traffic density measures than the other exposure assessment methods.We generally confirmed that traffic-related air pollution was associated with adverse reproductive outcomes regardless of the exposure assessment method employed, yet the size of the estimated effect depended on how both temporal and spatial variations were incorporated into exposure assessment. The LUR model was not transferable even between two contiguous areas within the same large metropolitan area in Southern California.
Project description:We used spatial analyses to examine exposure of people in vulnerable occupational groups to neighborhood-level environmental pollutants in the Bronx borough of New York City. Five-year estimates of environmental ambient exposures (derived from land use regression models for PM2.5 [particulate matter with an aerodynamic diameter ?2.5 µm] and black carbon) and demographic and occupational variables were harmonized at the census tract level. Correlations revealed that areas with high environmental exposures also had high proportions of people in service industries and manufacturing and high proportions of socioeconomically vulnerable populations. This combination of vulnerabilities may be cumulative, suggesting residents could have high occupational and residential exposures in addition to sociodemographic-related inequity.
Project description:BACKGROUND:Long-term exposure to ambient particulate matter (PM) has been previously linked with higher risk of cardiovascular events. This association may be mediated, at least partly, by increasing the risk of incident hypertension, a key determinant of cardiovascular risk. However, whether long-term exposure to PM is associated with incident hypertension remains unclear. METHODS:Using national geostatistical models incorporating geographic covariates and spatial smoothing, we estimated annual average concentrations of residential fine (PM2.5), respirable (PM10), and course (PM10-2.5) fractions of particulate matter among 44,255 post-menopausal women free of hypertension enrolled in the Women's Health Initiative (WHI) clinical trials. We used time-varying Cox proportional hazards models to evaluate the association between long-term average residential pollutant concentrations and incident hypertension, adjusting for potential confounding by sociodemographic factors, medical history, neighborhood socioeconomic measures, WHI study clinical site, clinical trial, and randomization arm. RESULTS:During 298,383 person-years of follow-up, 14,511 participants developed incident hypertension. The adjusted hazard ratios per interquartile range (IQR) increase in PM2.5, PM10, and PM10-2.5 were 1.13 (95% CI: 1.08, 1.17), 1.06 (1.03, 1.10), and 1.01 (95% CI: 0.97, 1.04), respectively. Statistically significant concentration-response relationships were identified for PM2.5 and PM10 fractions. The association between PM2.5 and hypertension was more pronounced among non-white participants and those residing in the Northeastern United States. CONCLUSIONS:In this cohort of post-menopausal women, ambient fine and respirable particulate matter exposures were associated with higher incidence rates of hypertension. These results suggest that particulate matter may be an important modifiable risk factor for hypertension.
Project description:BACKGROUND:The current single-pollutant approach to regulating ambient air pollutants is effective at protecting public health, but efficiencies may be gained by addressing issues in a multipollutant context since multiple pollutants often have common sources and individuals are exposed to more than one pollutant at a time. OBJECTIVE:We performed a cross-disciplinary review of the effects of multipollutant exposures on cardiovascular effects. METHODS:A broad literature search for references including at least two criteria air pollutants (particulate matter [PM], ozone [O3], oxides of nitrogen, sulfur oxides, carbon monoxide) was conducted. References were culled based on scientific discipline then searched for terms related to cardiovascular disease. Most multipollutant epidemiologic and experimental (i.e., controlled human exposure, animal toxicology) studies examined PM and O3 together. DISCUSSION:Epidemiologic and experimental studies provide some evidence for O3 concentration modifying the effect of PM, although PM did not modify O3 risk estimates. Experimental studies of combined exposure to PM and O3 provided evidence for additivity, synergism, and/or antagonism depending on the specific health endpoint. Evidence for other pollutant pairs was more limited. CONCLUSIONS:Overall, the evidence for multipollutant effects was often heterogeneous, and the limited number of studies inhibited making a conclusion about the nature of the relationship between pollutant combinations and cardiovascular disease.
Project description:BACKGROUND: The health effects of particulate air pollution are widely recognized and there is some evidence that the magnitude of these effects vary by particle component. We studied the effects of ambient fine particles (aerodynamic diameter < 2.5 ?m, PM(2.5)) and their components on cause-specific mortality in Santiago, Chile, where particulate pollution is a major public health concern. METHODS: Air pollution was collected in a residential area in the center of Santiago. Daily mortality counts were obtained from the National Institute of Statistic. The associations between PM(2.5) and cause-specific mortality were studied by time series analysis controlling for time trends, day of the week, temperature and relative humidity. We then included an interaction term between PM(2.5) and the monthly averages of the mean ratios of individual elements to PM2.5 mass. RESULTS: We found significant effects of PM(2.5) on all the causes analyzed, with a 1.33% increase (95% CI: 0.87-1.78) in cardiovascular mortality per 10 ?g/m(3) increase in the two days average of PM(2.5). We found that zinc was associated with higher cardiovascular mortality. Particles with high content of chromium, copper and sulfur showed stronger associations with respiratory and COPD mortality, while high zinc and sodium content of PM(2.5) amplified the association with cerebrovascular disease. CONCLUSIONS: Our findings suggest that PM(2.5) with high zinc, chromium, copper, sodium, and sulfur content have stronger associations with mortality than PM(2.5) mass alone in Santiago, Chile. The sources of particles containing these elements need to be determined to better control their emissions.