Background Particulate air pollution has been linked toheart disease and stroke, possibly resulting from enhanced coagulationand arterial thrombosis. Whether particulate air pollution exposureis related to venous thrombosis is unknown.
Methods We examined the association of exposure to particulatematter of less than 10 µm in aerodynamic diameter (PM10)with deep vein thrombosis (DVT) risk in 870 patients and 1210controls from the Lombardy region in Italy, who were examinedbetween 1995 and 2005. We estimated exposure to PM10 in theyear before DVT diagnosis (cases) or examination (controls)through area-specific mean levels obtained from ambient monitors.
Results Higher mean PM10 level in the year before theexamination was associated with shortened prothrombin time (PT)in DVT cases (standardized regression coefficient [β] = –0.12;95% confidence interval [CI], –0.23 to 0.00) (P = .04)and controls (β = –0.06; 95% CI, –0.11to 0.00) (P = .04). Each increase of 10 µg/m3in PM10 was associated with a 70% increase in DVT risk (oddsratio [OR], 1.70; 95% CI, 1.30 to 2.23) (P < .001)in models adjusting for clinical and environmental covariates.The exposure-response relationship was approximately linearover the observed PM10 range. The association between PM10 leveland DVT risk was weaker in women (OR, 1.40; 95% CI, 1.02 to1.92) (P = .02 for the interaction between PM10 andsex), particularly in those using oral contraceptives or hormonetherapy (OR, 0.97; 95% CI, 0.58 to 1.61) (P = .048for the interaction between PM10 level and hormone use).
Conclusions Long-term exposure to particulate air pollutionis associated with altered coagulation function and DVT risk.Other risk factors for DVT may modulate the effect of particulate air pollution.
Exposure to particulate air pollution has been associated withincreased short- and long-term morbidity and mortality fromheart disease and stroke.1-4 Hypercoagulability and enhancedthrombosis have been indicated as one mechanistic pathway thatmediates such effects,4-5proteins such as factor VIII, von Willebrand factor, and fibrinogenhave been associated with the exposure.5-7 Recently, changesin coagulation function resulting in shortened prothrombin time(PT) have been observed in association with higher mean levelof particulate air pollution of less than 10 µm in aerodynamicdiameter (PM10) in the 30 days before the examination, suggestingthat extended PM10 exposure may cause effects on blood clotting since higher plasma levels of coagulation.8Procoagulant abnormalities are stronger determinants of venousthan of arterial thrombosis,9 and increased risk of deep veinthrombosis (DVT) has been associated with a series of heritableor acquired risk factors that cause hypercoagulability, includingfactor V Leiden and G20210A prothrombin mutations, deficienciesof the natural anticoagulant proteins antithrombin, proteinC and protein S, and use of oral contraceptive or hormone therapy.10-11In rat and hamster models developed to investigate mechanismsinvolved in arterial thrombosis, inhalation or intravenous administrationof air pollution constituents—such as diesel exhaustsand ultrafine particles—induces thrombosis of the femoral6and ear veins.12 In human subjects, to our knowledge, no evidenceis currently available relating air pollution exposure to DVT.In the present study, we investigated whether long-term ambientPM10 exposure was associated with increased thrombotic susceptibilityand higher DVT risk in a large epidemiologic investigation conductedin the Lombardy region in northern Italy. METHODS
Figure 1. Map of the Lombardy region (Italy) showing the location of the 53 air pollution monitors in the 9 areas identified for the study.
STATISTICAL ANALYSIS In previous work, we tested the association of shorter-termPM10 exposure with PT and aPTT in the same healthy subjectswho served as controls in the present analysis.13 In the presentstudy, to evaluate the association between PM10 and PT and aPTTbetween DVT cases or controls, we used the same statisticalmethods we previously described.13 Differences between cases and controls after stratificationby geographic area or study period were tested using the Mantel-Haenszelmethod. The association of PM10 level with DVT risk was testedin a case-control analysis using unconditional logistic regressionmodels including, as independent variables, sex, area of residence,education (elementary/middle school, high school, college),factor V Leiden or G20210A prothrombin mutation (yes/no), andcurrent use of oral contraceptives or hormone therapy (yes/no).Variables with potentially nonlinear associations with risk,including age, body mass index, day of the year (for seasonality),index date (for long-term time trends), and ambient temperature,were controlled using penalized regression splines with 4 dffor each variable.15 Unconditional regression was performedto allow for the use of penalized splines, which are not availablefor use in conditional logistic models in available softwarepackages, as well as to avoid the loss from the analyses ofsubjects in incomplete sets due to participation refusal ormissing exposure or covariate information. As approximationof the relative risk of DVT, we reported odds ratios (ORs) and95% confidence intervals (CIs) for each increase of 10 µg/m3in the mean level of PM10. We used Stata version 9.0 (StataCorp,College Station, Texas) for descriptive analyses and R version2.2.0 (R Project for Statistical Computing, Vienna, Austria)to fit regression models. All statistical tests were 2 sided,and P < .05 was considered statistically significant. RESULTS
CHARACTERISTICS OF THE STUDY POPULATIONTable 1 gives the characteristics of the 871 DVT cases (420men and 451 women) and 1210 controls (490 men and 720 women).Cases and controls had similar distributions by age (P = .12)and area of residence (P = .59). Cases had higherbody mass index (P < .001); lower education (P = .01);more frequent use of oral contraceptives or hormone therapy(P < .001); and higher prevalences of factor VLeiden (P < .001), G20210 prothrombin mutation(P < .001), inherited deficiencies of natural anticoagulantproteins (P < .001), hyperhomocysteinemia (P < .001),and any of the causes of thrombophilia (P < .001).Controls were less likely to be examined for the study duringthe summer and their examinations were more frequent in thefall, whereas no major seasonal pattern was found for DVT diagnoses(P < .001). Mean ambient temperatures were higheron the days of diagnosis of DVT cases than on the days of examinationof controls (P < .001). A larger proportion ofcontrols were entered earlier in the study compared with cases(P < .001). This difference in recruitment wasaccounted for by performing analyses stratified by year andthrough the use of nonlinear terms for long-time trends in multivariablemodels.
Table 2. Estimated Changes of PT and aPTT Associated With PM10 Levels in the Year Before the Examination in DVT Cases and Controls
PARTICLE EXPOSURE AND RELATIVE RISK OF DVT Table 3 presents the tertiles of the mean PM10 level measuredin the area of residence during the year before the date ofDVT diagnosis (cases) or date of examination (controls), accordingto their area of residence and year of study. In both casesand controls, PM10 level was highest in the Milan urban andsuburban areas (P < .001). Subjects from the Alpineterritory and the lower Valtellina Valley were all in the lowesttertile of PM10 exposure. In both cases and controls, the frequencyof subjects being in the highest tertile of PM10 exposure washighest in the earlier years of the study, and it decreasedthroughout the study period, to reach the lowest frequency inthe most recent years (P < .001).
Figure 2. Level of exposure to fine particulate matter and the risk of deep vein thrombosis (DVT). The graph demonstrates the observed relationship between the relative risk of DVT and the level of particulate matter of less than 10 µm in aerodynamic diameter (PM10) in the year preceding the diagnosis. These results suggest a linear relationship between exposure and risk, though the 95% confidence intervals (shaded areas) are wide at the extremes of exposure. Risk is depicted in comparison with a reference value of 12.0 µg/m3 (minimum observed PM10 level). The histogram in the bottom part illustrates the density of exposure distribution for air pollution. Risk estimates are adjusted for age, sex, year of diagnosis, area of residence, body mass index, education, current use of oral contraceptives or hormone therapy, Leiden V or prothrombin mutations, season, and ambient temperature.
Table 4. Relative Riska of Deep Vein Thrombosis (DVT) Associated With a 10 µg/m3 Increase in PM10 in the Year Preceding the Diagnosis by Subjects’ Characteristics
SENSITIVITY ANALYSES We repeated all the analyses after excluding cases with a recurrent(nonfirst) episode of DVT (n = 110). Risk estimateswere very similar to those for the entire study population.Each increase of 10 µg/m3 in PM10 level was associatedwith an OR of 1.67 (95% CI, 1.27 to 2.22) (P < .001),adjusting for multiple variables. In the subsample of 760 caseswith a single episode of DVT, the variations in the associationbetween PM10 level and the risk of DVT due to demographic characteristics,presence of thrombophilia, or use of hormone therapies weresimilar to those observed in the entire study population. To evaluate the influence of splines selection in fitting nonlinerterms in the logistic models, we repeated all statistical analysesby using natural splines instead of penalized splines. The useof natural splines did not modify the statistical significanceof the results, with only small changes in the risk estimates. We also evaluated the influence of different methods for adjustingfor long-term time trends during the study period (supplementaryTable 2; available at: http://www.cdldevoto.it/didattic/materiale/Appendix_Archives_online.pdf).As was shown in the subsection "Particle Exposure and RelativeRisk of DVT," ignoring long-term time trends in the analyseswould have almost completely obscured the association betweenPM10 level and DVT risk. However, all of the methods for adjustmentfor long-term time trends that we evaluated in our sensitivityanalysis (fitting dummy variables for each year of the studyperiod, as well as linear terms or penalized splines for indexdate with degrees of freedom varying between 2 and 8) producedrisk estimates indicating a significant association betweenPM10 level and DVT risk, with only small changes due to differenthandling of the time trends for most of the methods. However,it is worth noting that using only a linear variable for thelong-term trend would have produced a lower OR, likely reflectingless than optimal fitting of the time relationships presentin our data. COMMENT
In this study of DVT cases and healthy controls, exposure toincreased concentrations of particulate air pollution in theyear before diagnosis was associated with increased DVT riskafter controlling for clinical and environmental covariates.Mean level of PM10 before the examination was also correlatedwith shorter PT in both cases and controls. The DVT risk increaseassociated with PM10 level was smaller in women and limitedto those who were not using oral contraceptives or hormone therapyat the time of diagnosis.Long-term exposure to particulate air pollution has been associatedwith increased risk of coronary heart and cerebrovascular diseasein multiple investigations conducted in several countries.4A systemic increase in thrombotic tendency, secondary to theinduction of inflammatory mediators produced in the lungs andreleased in the circulation or to the translocation of particlesof smaller diameter from the lungs into the circulation6 hasbeen frequently proposed to account for the cardiac and cerebrovasculareffects of particulate air pollution. In contrast, venous thrombosishas received little attention in studies on the cardiovascularoutcomes of air pollution. In a time-series analysis from theNetherlands, Hoek et al16 reported an association of short-termexposure to ambient ozone and, to a lesser extent, black smokeand PM10, with increased mortality from embolism and thrombosis,a broad category that included arterial and venous thrombosesin various sites. To date, no study has specifically addressedthe association between particulate air pollution and DVT. Inour population, we estimated an overall 70% increase in DVTrisk with each increase of 10 µg/m3 in PM10 level duringthe year before diagnosis. For comparison, in the Harvard SixCities Study, the risk of death from cardiopulmonary diseaseswas 37% higher in the most polluted compared with the leastpolluted cities.1 In the Women’s Health Initiative Study,an increase of 10 µg/m3 of annual mean concentrationsof PM2.5, which is considered a stronger predictor than PM10level of air pollution effects, was associated with a 24% increasein the risk of cardiovascular events and a 76% increase in therisk of death from cardiovascular disease.2 The estimated increasein risk of death from all cardiovascular causes associated with10 µg/m3 elevation in long-term PM2.5 level was 19% inthe Harvard Six Cities study and 13% in the study by the AmericanCancer Society.3 In the present study, PM10 exposure did not increase the riskof DVT in women as much as in men. By evaluating additionalrisk factors, we found that part—if not all—of suchrisk attenuation was due to the lack of association betweenPM10 level and the risk of DVT among women using oral contraceptivesor hormone therapy. Such hormone therapies are independent riskfactors for DVT,10 which is also confirmed in this study bythe higher prevalence of oral contraceptive and hormone usein the cases compared with the controls. Use of oral contraceptivesand hormone therapy induces changes in coagulation factors,such as increased levels of the procoagulant factors VII, IX,X, XII, and XIII, von Willebrand factor, and fibrinogen andreduced levels of the anticoagulant proteins antithrombin andprotein S,13, 17-18 that are similar in characteristics anddegree to the coagulation changes observed after exposure toair particles.7-8,19-22 We surmise that prothrombotic mechanismsare already activated in those receiving hormone therapy sothat they undergo less or no further induction after air particleexposure. In our analyses, we evaluated DVT risk in association with thelevel of PM10 measured during the year before diagnosis. Inthis study, the use of short-term (hourly or daily) air pollutionlevels would not have been appropriate because DVT presentationis often subtle and its diagnosis has been shown to lag as longas 4 weeks after the initial DVT symptoms.23 In the presentwork, we demonstrated that mean PM10 level in the year beforethe examination was associated with shortened PT, extendingour previous observation of an association with shorter exposuretime windows.13 Interestingly, while the negative effects ofmean PM10 levels on PT were independent of the time-window selected,the 1-year mean PM10 was the only exposure metric significantlyassociated with shortened PT among the cases. In addition, whilein our previous work we could not find any relation between30-day mean PM10 level and aPTT, in our present study, a nonsignificant(P = .07) association was observed between aPTT shorteningand 1-year mean PM10 among the controls. This association, takentogether with the similar PT change, suggests that 1-year PM10exposure may also affect aPTT. Thus, the use of PM10 level inthe year before diagnosis appeared to capture a fuller rangeof prothrombotic effects, while also reducing the risks of confoundingby seasonal patterns and ambient temperature. This study hasthe advantage of being based on a large number of DVT casesand controls recruited using a standardized protocol over along time span. Cases had objective diagnoses of DVT, and bothcases and controls were well characterized for inherited andacquired risk factors for DVT. In the statistical analysis,we used models that included nonlinear regression terms to adjustfor long-term time trends and day of the year (thus controllingfor confounding from year of the study and seasonal variations),in addition to age, sex, area of residence, education, factorV Leiden, G20210A prothrombin mutation, use of oral contraceptiveor hormone therapy, body mass index, and ambient temperature. Because the healthy controls were selected among nonblood relativesand friends of the DVT cases, they tended to be distributedin the 9 study areas, with proportions that were very similarto those of the DVT cases. This might have generated overmatchingin our study, ie, the exposure levels of controls may have beenmore similar to those of DVT cases than they actually are inthe population at risk. Therefore, it is possible that riskestimates were underestimated in our study. A limitation ofthis study is that we used ambient air pollution estimated atthe subjects' address as a surrogate for personal exposure,which may have resulted in measurement error, since most subjectsconduct a large part of their daily activities away from theirresidence. A detailed questionnaire was used to ascertain knownrisk factors for DVT, but no information was collected concerningdaily activities, such as time spent outside or in traffic,that could have refined the assessment of PM10 exposure. Inaddition, our exposure assessment was done by dividing the Lombardyregion into 9 areas for which mean PM10 levels were assignedby averaging measurements from multiple monitors. Although theseareas were selected to group together territories with similarpopulation densities and geographical characteristics, thuslikely reducing within-area variations of the exposure, we werenot able to obtain PM10 level estimates at a smaller scale.However, PM10 levels tend to be spatially homogeneous, and arecent study comparing personal exposures with site monitoringin Boston, Massachusetts, reported that monitor readings andpersonal exposure are highly correlated.24 In addition, it hasbeen shown that using ambient measures to estimate individualexposure is likely to produce an underestimation of pollutioneffects25 rather than causing the increased risk of DVT foundin our study population. In conclusion, this study provides evidence in support of anassociation of exposure to particulate air pollution with enhancedprothrombotic mechanisms and risk of DVT. Given the magnitudeof the observed effects and the widespread diffusion of particulatepollutants, our findings introduce a novel and common risk factorinto the pathogenesis of DVT and, at the same time, give furthersubstance to the call for tighter standards and continued effortsaimed at reducing the impact of urban air pollutants on humanhealth. AUTHOR INFORMATION
Correspondence: Andrea Baccarelli, MD, PhD, Exposure, Epidemiology,and Risk Program, Harvard School of Public Health, 401 ParkDr, Landmark Center, Ste 415G W, PO Box 15698, Boston, MA 02215(email@example.com ).Accepted for Publication: December 14, 2007. Author Contributions:Study concept and design: Baccarelli,Martinelli, Bertazzi, Mannucci, and Schwartz. Acquisition ofdata: Baccarelli, Martinelli, Zanobetti, and Grillo. Analysisand interpretation of data: Baccarelli, Martinelli, Zanobetti,Grillo, Hou, Bertazzi, and Schwartz. Drafting of the manuscript:Baccarelli, Hou, Mannucci, and Schwartz. Critical revision ofthe manuscript for important intellectual content: Martinelli,Zanobetti, Grillo, Bertazzi, and Schwartz. Statistical analysis:Baccarelli, Zanobetti, Grillo, and Schwartz. Obtained funding:Baccarelli,Bertazzi, and Schwartz. Study supervision: Baccarelli, Hou,Bertazzi, and Mannucci. Financial Disclosure: None reported. Funding/Support: This work was supported by grants R83241601and R827353 from the Environmental Protection Agency ParticulateMatter Center; grants ES0002 and ES015172-01 and grant PO1 ES009825from the National Institute of Environmental Health Sciences;grant 2004-2006/97-C from the MIUR (Ministero dell'Istruzione,dell'Università e della Ricerca) InternationalizationProgram; and grants UniMi 8614/2006 and UniMi 9167/2007 fromtheCARIPLO (Cassa di Risparmio delle Provincie Lombarde) Foundationand Lombardy region. Additional Contributions: Guido Lanzani, PhD, Nadia Carfagno,BSPH, and Anna Cazzullo, MS, ARPA Lombardia, provided supportin air-monitoring data handling; and Steve Melly, MS, HarvardSchool of Public Health, assisted in the creation of geographicmaps. This article was corrected for typographical errors on 5/12/2008. Author Affiliations: Exposure, Epidemiology, and Risk Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts (Drs Baccarelli, Zanobetti, and Schwartz); Departments of Preventive Medicine and Environmental and Occupational Health (Drs Baccarelli, Grillo, and Bertazzi), and A. Bianchi Bonomi Haemophilia and Thrombosis Center, Department of Medicine and Medical Specialties (Drs Martinelli and Mannucci), University of Milan and IRCCS (Istituto di Ricovero e Cura a Carattere Scientifico) Maggiore Hospital, Mangiagalli and Regina Elena Foundation, Milan, Italy; and Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois (Dr Hou). REFERENCES
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