November 21, 2008

Energy Answers Big Lies

Energy Answers and Big Lies

" Die Engländer gehen nach dem Prinzip vor,
wenn du lügst, dann lüge gründlich,
und vor allem bleibe bei dem, was du gelogen hast! "

"Aus Churchills Lügenfabrik"


DCC apparently used 19,000,000 Euro and The Big Lie method when acting for Covanta during the Poolbeg Waste-To-Toxins Oral hearings.

Escaping US Law?

The proposed Covanta operation at Poolbeg has its HQ in Luxembourg – presumably to firewall it from public liability for 100,000 premature deaths. Covanta also controls Energy Answers International, the organisation now proposing a Waste-To-Toxins incinerator in West Dublin at Rathcoole. This Energy Answers operation is firewalled in The Virgin Islands, not so far from GITMO. Enron, another "Energy" corporation also had multiple special purpose operations in the Caribbean before it managed itself into one of the largest bankruptcies in history. Why are they all afraid of US Jurisprudence?

Apparently these Waste-To-Toxins proposers are using some of the same Big Lies at Poolbeg and at Rathcoole.

Covanta and Energy Answers employ a 10-year-Ex-EPA-Ireland Director as a “consultant”.

Some informed responses to the cynical Big Lies deployed for the proposed Waste-To-Toxins factory at Rathcoole are below.

The Biodiversity Big Lie - Response

Consultant ecologist Mieke Muyllaert said the site was "of greater biodiversity significance than suggested by the environmental impact statement".

The Transportation Big Lie - Response

Transportation expert Christy O'Sullivan said there were significant dangers posed for traffic on the N7.

The Toxins Big Lie - Response

Biochemist Deborah McDermott was incredulous that the applicant had claimed the boiler ash did not qualify as hazardous waste.

The Landscape Big Lie - Response

Rónán Mac Diarmada, an agricultural scientist, said the drawings in the application were flawed. "The landscape drawing is unsatisfactory in terms of detail and accuracy. The site boundary does not correlate with other consultants' drawings. The site layout does not show levels and does not correspond to engineers' drawings."


November 20, 2008

Sweden's Incinerators Forced to Import 600,000 Tonnes Waste

November 20, 2008
Sweden is an educated and advanced society without the corruption and class divisions exploited by Ireland's political class. Swedes trust "Lisbon". Guess why "Paddy" doesn't.

So its possible Sweden could run an incinerator in an honest manner. An incinerator run by Swedes is possibly not a scary thing, with just a few premature deaths a year. This
acceptable level is not unlike the people riding bicycles in Dublin, otherwise known as the kidney-donors (Sweden has real bicycle paths). In starkest contrast, an incinerator run by Dublin City Council is a very scary thing indeed. DCC's level of honesty means they can not even run their 'Ringsend' schijt factory. However it seems even Sweden has slipped into the gombeen land of Abba's money.

Cynically, for its
proposed Waste-To-Toxins incinerator at Poolbeg, the DCC team exploits Irish class divisions along with insular jackeen-culchie perspectives. In other words, the "republican party" Fianna-Fail seems to be continuing British tactics to exploit Ireland. The fat boys from New Jersey are laughing all the way to their Caribbean banks. And they are fat - their Vice President had to use the elevators to go up one floor at The Gresham.

"Never Misunderestimate The Stupidity of the People We Serve."

This is a common phrase in California.

Dublin City Council is building on its world-class legacy where it turned the beach at Sandymount-Irishtown-Ringsend into Dublin's rubbish dump.
Can Dublin City Council and Covanta now turn Ireland into Europe's garbage dump? This would displace socialist and green Sweden from the honour of being Europe's garbage dump.

Sverige - Europas soptipp

Say it in Swedish

Celtic Tiger Johnny Logan liberated Europe from the greed of Abba's Money, Money, Money.

Sweden Reduced To Importing Garbage

Scavenging at Högdalen CHP. Photo Bjorn Larsson Ash / Scanpix

High profit in the Swedish Waste-To-Toxins incineration business has led to overcapacity, which now must be filled with the import of waste from other countries. According to the Swedish Society for Nature Conservation Sweden is in danger of becoming Europe's garbage dump.

" Swedish incineration plants are among the best in Europe,

so we can become a YOUNG CUCKOO in other countries in that

we attract the waste and create a market for incineration, "

said Svante Axelsson, Secretary General of Swedish Society for Nature Conservation.

Is there a risk that Sweden is Europe's garbage dump?

Yes, there is.

20 november 2008

Sverige tvingas importera sopor

Sedan år 2000 har antalet förbränningsanläggningar för avfall mer än fördubblats i Sverige. Och den lönsamhet som finns i förbränningsbranschen har lett till överkapacitet som nu måste fyllas ut med import av avfall från andra länder. Enligt Naturskyddsföreningen riskerar Sverige att bli Europas soptipp, men branschorganisationen håller inte med.

– De svenska förbränningsanläggningarna är bland de bättre i Europa, så vi kan bli en gökunge i andra länder genom att vi attraherar avfall och skapar en marknad för förbränning, säger Svante Axelsson, generalsekreterare på Svenska Naturskyddsföreningen.

Finns det en risk för att Sverige blir Europas soptipp?

– Ja, det finns det.


Zana Schiroyi

Anna Nyström, SR Örebro


Victoria Gaunitz

Magdalena Martinsson, SR Norrbotten

November 19, 2008

Toxic Slag Permitted by Mr. Gormley's DDDA At Nature Site?

Apparently the Dublin Docklands Developers Authority has authorised the dumping of a mountain of potentially toxic slag beside Irishtown Nature Park. Apparently the EPA is toothless, indifferent and possibly even criminally negligent(a).

John Gormley, July 18, 2005. JG/RM.
Planning Application 4996/04

Following the Poolbeg Incinerator oral hearings the Bord Pleanala Inspector reported pollution from particles in Poolbeg was already at or above acceptable legal norms. The Inspector specified measures should be taken to reduce particle pollution during construction. So now, even before final approval from their EPA buddies on behalf of foreign corporations, DDDA+DCC is breaking this condition. With this reckless attitude why would DCC control invisible dioxins?

From Irishtown Nature Park.
November 2008.

The Dublin Docklands Developers Authority is a taxpayer funded quango in Mr J. Gormleys's control. The quango is used to perform Chinese style autocratic urban planning. For instance, the quango prevents access to the Bord Pleanala planning process by educated citizens. The quango hides information from the public.

Dumping the potentially toxic slag may be a pre-emptive action by DDDA+DCC or others to destroy the land used by Brent Geese (fresh water, flight paths). The reckless and possibly illegal work appears to be in advance of authorisation from their cronies in EPA-Ireland for a Waste-To-Toxins incinerator. Apparently EPA-Ireland will not investigate the "sand" - the fine public protectors first require a piece of paper, their usual excuse apparently.

Invisible 'fine particles' from this 80 foot high mountain blow over Sandymount, Irishtown and Ringsend damaging human health. But DCC & DDDA will say "you can not prove that".

DCC's sewage factory stinks and wastes tens of millions of emergency tax-payer cash, signed for by Mr J Gormley in November 2008. Whether this unforseeable situation is due to corruption or bad engineering by DCC is an open question. However DCC is used to engineering schijt.

An efficiently managed Waste-To-Toxins incinerator would reduce life by 100,000 man-years in its first 15 years [British Society for Ecological Medicine]. An ineptly or possibly corruptly managed Waste-To-Toxins incinerator will cause tens to hundreds of premature deaths across Dublin, each year. Do you trust DCC with your life expectancy? Do you trust Covanta, a corporation with a curious regard for obeying the law in its home state of New Jersey.

(a) The EPA CharadeThe Philadelphia Inquirer's been running a good series about the toothless, indifferent and possibly even criminally negligent EPA.

Please send any insights or validated corrections to

Deadly Particles (PM2.5), Dublin Bay Incinerator, Dublin Docklands Authority, Gormley, Health, Law Breaking, PM2.5, Poolbeg Incinerator

November 11, 2008

No more incinerators should be approved - British Society for Ecological Medicine - June 2008

June 2008
The British Society for Ecological Medicine concludes
that no more incinerators should be approved.

Recent research, including that relating to fine and ultrafine particulates, the costs of incineration, together with research investigating nonstandard emissions from incinerators, has demonstrated that the hazards of incineration are greater than previously realised.

The accumulated evidence on
the health risks of incinerators is simply too strong to ignore and their use cannot be justified now that better, cheaper and far less hazardous methods of waste disposal have become available.

The Health Effects of Waste Incinerators
4th Report of the British Society for
Ecological Medicine
Second Edition June 2008
Moderators: Dr Jeremy Thompson and Dr Honor Anthony.


Executive Summary

· Large studies have shown higher rates of adult and childhood cancer and also
birth defects around municipal waste incinerators: the results are consistent
with the associations being causal. A number of smaller epidemiological
studies support this interpretation and suggest that the range of illnesses
produced by incinerators may be much wider.

· Incinerator emissions are a major source of fine particulates, of toxic metals
and of more than 200 organic chemicals, including known carcinogens,
mutagens, and hormone disrupters. Emissions also contain other unidentified
compounds whose potential for harm is as yet unknown, as was once the case
with dioxins. Since the nature of waste is continually changing, so is the
chemical nature of the incinerator emissions and therefore the potential for
adverse health effects.

· Present safety measures are designed to avoid acute toxic effects in the
immediate neighbourhood, but ignore the fact that many of the pollutants
bioaccumulate, enter the food chain and can cause chronic illnesses over time
and over a much wider geographical area. No official attempts have been
made to assess the effects of emissions on long-term health.

· Incinerators produce bottom and fly ash which amount to 30-50% by volume
of the original waste (if compacted), and require transportation to landfill
sites. Abatement equipment in modern incinerators merely transfers the toxic
load, notably that of dioxins and heavy metals, from airborne emissions to the
fly ash. This fly ash is light, readily windborne and mostly of low particle size.
It represents a considerable and poorly understood health hazard.

· Two large cohort studies in America have shown that fine (PM2.5) particulate
air pollution causes increases in all-cause mortality, cardiovascular mortality
and mortality from lung cancer, after adjustment for other factors. A more
recent, well-designed study of morbidity and mortality in postmenopausal
women has confirmed this, showing a 76% increase in cardiovascular and
83% increase in cerebrovascular mortality in women exposed to higher levels
of fine particulates. These fine particulates are primarily produced by
combustion processes and are emitted in large quantities by incinerators.

· Higher levels of fine particulates have been associated with an increased
prevalence of asthma and COPD.

· Fine particulates formed in incinerators in the presence of toxic metals and
organic toxins (including those known to be carcinogens), adsorb these
pollutants and carry them into the blood stream and into the cells of the body.

· Toxic metals accumulate in the body and have been implicated in a range of
emotional and behavioural problems in children including autism, dyslexia,
attention deficit and hyperactivity disorder (ADHD), learning difficulties, and
delinquency, and in problems in adults including violence, dementia,
depression and Parkinson’s disease. Increased rates of autism and learning
disabilities have been noted to occur around sites that release mercury into the
environment. Toxic metals are universally present in incinerator emissions and
present in high concentrations in the fly ash.

· Susceptibility to chemical pollutants varies, depending on genetic and
acquired factors, with the maximum impact being on the foetus. Acute exposure
can lead to sensitisation of some individuals, leaving them with lifelong

low dose chemical sensitivity.

· Few chemical combinations have been tested for toxicity, even though
synergistic effects have been demonstrated in the majority of cases when this
testing has been done. This synergy could greatly increase the toxicity of the
pollutants emitted, but this danger has not been assessed.

· Both cancer and asthma have increased relentlessly along with
industrialisation, and cancer rates have been shown to correlate geographically
with both toxic waste treatment facilities and the presence of chemical
industries, pointing to an urgent need to reduce our exposure.

· In the UK, some incinerators burn radioactive material producing radioactive
particulates. Inhalation allows entry into the body of this radioactive material
which can subsequently emit alpha or beta radiation. This type of radiation has
low danger outside the body but is highly destructive within. No studies have
been done to assess the danger to health of these radioactive emissions.

· Some chemical pollutants such as polyaromatic hydrocarbons (PAHs) and
heavy metals are known to cause genetic changes. This represents not only a
risk to present generations but to future generations.

· Monitoring of incinerators has been unsatisfactory in the lack of rigor, the
infrequency of monitoring, the small number of compounds measured, the
levels deemed acceptable, and the absence of biological monitoring. Approval
of new installations has depended on modelling data, supposed to be scientific
measures of safety, even though the method used has no more than a 30%
accuracy of predicting pollutants levels correctly and ignores the important
problems of secondary particulates and chemical interactions.

· It has been claimed that modern abatement procedures render the emissions
from incinerators safe, but this is impossible to establish and would apply only
to emissions generated under standard operating conditions. Of much more
concern are non-standard operating conditions including start-up and shutdown
when large volumes of pollutants are released within a short period of
time. Two of the most hazardous emissions – fine particulates and heavy
metals – are relatively resistant to removal.

· The safety of new incinerator installations cannot be established in advance
and, although rigorous independent health monitoring might give rise to
suspicions of adverse effects on the foetus and infant within a few years, this
type of monitoring has not been put in place, and in the short term would not
reach statistical significance for individual installations. Other effects, such as
adult cancers, could be delayed for at least ten to twenty years. It would
therefore be appropriate to apply the precautionary principle here.

· There are now alternative methods of dealing with waste which would avoid
the main health hazards of incineration, would produce more energy and
would be far cheaper in real terms, if the health costs were taken into account.

· Incinerators presently contravene basic human rights as stated by the United
Nations Commission on Human Rights, in particular the Right to Life under
the European Human Rights Convention, but also the Stockholm Convention
and the Environmental Protection Act of 1990. The foetus, infant and child
are most at risk from incinerator emissions: their rights are therefore being
ignored and violated, which is not in keeping with the concept of a just society. Nor is the present policy of locating incinerators in deprived areas
where their health effects will be maximal: this needs urgent review.

· Reviewing the literature for the second edition has confirmed our earlier
conclusions. Recent research, including that relating to fine and ultrafine
particulates, the costs of incineration, together with research investigating nonstandard
emissions from incinerators, has demonstrated that the hazards of
incineration are greater than previously realised. The accumulated evidence on
the health risks of incinerators is simply too strong to ignore and their use
cannot be justified now that better, cheaper and far less hazardous methods of
waste disposal have become available. We therefore conclude that no more
incinerators should be approved.

Air Pollution and Deep Vein Thrombosis. [Baccarelli]

Particulate air pollution has been linked to heart disease and stroke.

Exposure to Particulate Air Pollution and Risk of Deep Vein Thrombosis Andrea Baccarelli, MD, PhD; Ida Martinelli, MD; Antonella Zanobetti, PhD; Paolo Grillo, MD; Li-Fang Hou, PhD; Pier A. Bertazzi, MD; Pier Mannuccio Mannucci, MD; Joel Schwartz, PhD

Arch Intern Med. 2008;168(9):920-927.

Background  Particulate air pollution has been linked to heart disease and stroke, possibly resulting from enhanced coagulation and arterial thrombosis. Whether particulate air pollution exposure is related to venous thrombosis is unknown.  

Methods  We examined the association of exposure to particulate matter of less than 10 µm in aerodynamic diameter (PM10) with deep vein thrombosis (DVT) risk in 870 patients and 1210 controls from the Lombardy region in Italy, who were examined between 1995 and 2005. We estimated exposure to PM10 in the year 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 the examination 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, –0.11 to 0.00) (P = .04). Each increase of 10 µg/m3 in PM10 was associated with a 70% increase in DVT risk (odds ratio [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 linear over the observed PM10 range. The association between PM10 level and DVT risk was weaker in women (OR, 1.40; 95% CI, 1.02 to 1.92) (P = .02 for the interaction between PM10 and sex), particularly in those using oral contraceptives or hormone therapy (OR, 0.97; 95% CI, 0.58 to 1.61) (P = .048 for the interaction between PM10 level and hormone use).

Conclusions  Long-term exposure to particulate air pollution is associated with altered coagulation function and DVT risk. Other risk factors for DVT may modulate the effect of particulate air pollution.




 Jump to Section
 •Author information

Exposure to particulate air pollution has been associated with increased short- and long-term morbidity and mortality from heart disease and stroke.1-4 Hypercoagulability and enhanced thrombosis have been indicated as one mechanistic pathway that mediates such effects,4-5 proteins such as factor VIII, von Willebrand factor, and fibrinogen have been associated with the exposure.5-7 Recently, changes in coagulation function resulting in shortened prothrombin time (PT) have been observed in association with higher mean level of particulate air pollution of less than 10 µm in aerodynamic diameter (PM10) in the 30 days before the examination, suggesting that extended PM10 exposure may cause effects on blood clotting since higher plasma levels of coagulation.8
Procoagulant abnormalities are stronger determinants of venous than of arterial thrombosis,9 and increased risk of deep vein thrombosis (DVT) has been associated with a series of heritable or acquired risk factors that cause hypercoagulability, including factor V Leiden and G20210A prothrombin mutations, deficiencies of the natural anticoagulant proteins antithrombin, protein C and protein S, and use of oral contraceptive or hormone therapy.10-11 In rat and hamster models developed to investigate mechanisms involved in arterial thrombosis, inhalation or intravenous administration of air pollution constituents—such as diesel exhausts and ultrafine particles—induces thrombosis of the femoral6 and ear veins.12 In human subjects, to our knowledge, no evidence is currently available relating air pollution exposure to DVT. In the present study, we investigated whether long-term ambient PM10 exposure was associated with increased thrombotic susceptibility and higher DVT risk in a large epidemiologic investigation conducted in the Lombardy region in northern Italy.


 Jump to Section
 •Author information

The cases included 871 patients (420 men and 451 women), who were Lombardy region residents and had been diagnosed between January 1995 through September 2005 as having lower limb DVT with or without symptomatic pulmonary embolism. Cases were referred to the Thrombosis Center, University of Milan, and IRCCS (Istituto di Ricovero e Cura a Carattere Scientifico) Maggiore Hospital, Milan, Italy, for a thrombophilia screening and were asked to bring all available clinical documentation. From this documentation, DVT was diagnosed based on evidence from objective methods such as compression ultrasonography or venography. Cases were asked about the presence of transient DVT risk factors in the month preceding the event, including surgery, trauma, immobilization (≥10 days), use of oral contraceptives or hormone therapy, and pregnancy or puerperium (6-week period after delivery). In 170 cases (19.5%), DVT was complicated by symptomatic pulmonary embolism. A total of 761 cases (84.4%) had a first DVT during the study period, whereas 110 (12.6%) had recurrent DVT. Cases with recurrent DVT had not been included in the study after their first diagnosis, since they were recruited after their first visit at the Thrombosis Center.
The controls included 1210 healthy Lombardy region residents (490 men and 720 women), who volunteered to be investigated at the Thrombosis Center in the same study period as the cases. The controls were recruited by asking each of the cases for a list of friends or nonblood relatives, and they were randomly selected from these lists using an algorithm that balanced the age distribution of the controls to that of the cases. To increase power to evaluate a potential effect modification by use of oral contraceptives and hormone therapy, female controls were recruited in excess of female cases. Thrombosis was excluded in controls with a structured questionnaire validated for the retrospective diagnosis of venous thromboembolism. Information on clinical, lifestyle, and reproductive factors was collected from all participants during an in-person interview. For practical reasons, because most of the interviews took place while the patients with DVT were in the hospital, interviewers could not be blinded to the case status. However, the subjects' addresses were confirmed on administrative or other official records, and exposure was assigned, based on the address, by a statistician blinded to the case status. Participants' written informed consents and local institutional review board approvals were obtained before the study. Prothrombin time and activated partial thromboplastin time (aPTT) were measured using laboratory methods previously described.13 Patients with DVT, if receiving anticoagulant drugs, were not asked to stop the treatment.
Methods for exposure assignment were previously described in detail.8, 14 Briefly, for each of the 9 geographic areas shown in Figure 1, mean concentrations of PM10 were computed using data from monitors located at 53 different sites throughout the Lombardy region. All participants were assigned to 1 of 9 geographic areas based on their residence at the time of the study.In our statistical analyses, PM10 level was evaluated using ambient PM10 concentrations averaged over the 365 days preceding the index date, also taking into account changes of residence during the same time window. Index dates were the date of diagnosis for DVT cases and the date of the examination for controls.

Figure 1
View larger version (82K):
[in this window]
[in a new window]
[as a PowerPoint slide]
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.

In previous work, we tested the association of shorter-term PM10 exposure with PT and aPTT in the same healthy subjects who served as controls in the present analysis.13 In the present study, to evaluate the association between PM10 and PT and aPTT between DVT cases or controls, we used the same statistical methods we previously described.13
Differences between cases and controls after stratification by geographic area or study period were tested using the Mantel-Haenszel method. The association of PM10 level with DVT risk was tested in a case-control analysis using unconditional logistic regression models including, as independent variables, sex, area of residence, education (elementary/middle school, high school, college), factor V Leiden or G20210A prothrombin mutation (yes/no), and current 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 df for each variable.15 Unconditional regression was performed to allow for the use of penalized splines, which are not available for use in conditional logistic models in available software packages, as well as to avoid the loss from the analyses of subjects in incomplete sets due to participation refusal or missing exposure or covariate information. As approximation of the relative risk of DVT, we reported odds ratios (ORs) and 95% confidence intervals (CIs) for each increase of 10 µg/m3 in the mean level of PM10. We used Stata version 9.0 (StataCorp, College Station, Texas) for descriptive analyses and R version 2.2.0 (R Project for Statistical Computing, Vienna, Austria) to fit regression models. All statistical tests were 2 sided, and P < .05 was considered statistically significant.


 Jump to Section
 •Author information

Table 1 gives the characteristics of the 871 DVT cases (420 men 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 higher body mass index (P < .001); lower education (P = .01); more frequent use of oral contraceptives or hormone therapy (P < .001); and higher prevalences of factor V Leiden (P < .001), G20210 prothrombin mutation (P < .001), inherited deficiencies of natural anticoagulant proteins (P < .001), hyperhomocysteinemia (P < .001), and any of the causes of thrombophilia (P < .001). Controls were less likely to be examined for the study during the summer and their examinations were more frequent in the fall, whereas no major seasonal pattern was found for DVT diagnoses (P < .001). Mean ambient temperatures were higher on the days of diagnosis of DVT cases than on the days of examination of controls (P < .001). A larger proportion of controls were entered earlier in the study compared with cases (P < .001). This difference in recruitment was accounted for by performing analyses stratified by year and through the use of nonlinear terms for long-time trends in multivariable models.

View this table:
[in this window]
[in a new window]
[as a PowerPoint slide]
Table 1. Characteristics of Deep Vein Thrombosis in Cases and Controls

Mean PM10 level over the 1 year before the examination was significantly associated with shortened PT in both cases (standardized regression coefficient [β] = –0.12; 95% CI, –0.23 to 0.00) (P = .04) and controls (β = –0.06; 95% CI –0.11 to 0.00) (P = .04). While the negative effects of mean PM10 levels on PT showed no major differences across means taken over 30, 60, 90, 180, or 270 days or 1 year (data not shown), the 1-year mean PM10 level was the only time window significantly associated with shortened PT among cases. A nonsignificant aPTT shortening was observed in association with the 1-year mean PM10 level among controls (β = –0.09; 95% CI, –0.19 to 0.01) (P = .07) but not in cases (β = 0.01; 95% CI, –0.03 to 0.04) (P = .78) (Table 2).

View this table:
[in this window]
[in a new window]
[as a PowerPoint slide]
Table 2. Estimated Changes of PT and aPTT Associated With PM10 Levels in the Year Before the Examination in DVT Cases and Controls

Table 3 presents the tertiles of the mean PM10 level measured in the area of residence during the year before the date of DVT diagnosis (cases) or date of examination (controls), according to their area of residence and year of study. In both cases and controls, PM10 level was highest in the Milan urban and suburban areas (P < .001). Subjects from the Alpine territory and the lower Valtellina Valley were all in the lowest tertile of PM10 exposure. In both cases and controls, the frequency of subjects being in the highest tertile of PM10 exposure was highest in the earlier years of the study, and it decreased throughout the study period, to reach the lowest frequency in the most recent years (P < .001).

View this table:
[in this window]
[in a new window]
[as a PowerPoint slide]
Table 3. Tertile of PM10 Exposure in DVT Cases and Controls by Area of Residence and Year of Examinationa

The DVT cases tended to have higher PM10 levels than the controls, and this pattern was more evident after the data were stratified by year of the study (Table 3). The test for the difference between cases and controls by tertile of PM10 level was significant in the analysis stratified by year of the study (P = .002, Mantel-Haenszel test). Such a difference was not statistically significant without stratification by year of the study (P = .44, Fisher exact test), indicating that inequalities in the distribution of cases and controls by study period, if not controlled, would have biased the results.
We estimated the relative risk of DVT associated with PM10 level in a multivariable model controlled 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. In this model, an increase of 10 µg/m3 in PM10 level was associated with an adjusted OR of 1.70 (95% CI, 1.30 to 2.23) (P < .001). The increase in DVT risk was nearly linear across the range of exposure concentrations that were measured (Figure 2).

Figure 2
View larger version (37K):
[in this window]
[in a new window]
[as a PowerPoint slide]
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.

We also examined DVT risk in association with different exposure time windows using PM10 level averaged over 90 days in the 2 years before diagnosis (see supplementary Figure 1 and supplementary Table 1; available at: Risk of DVT increased progressively with the duration of the time window evaluated and was statistically significant in association with the 270-day, 1-year, and 2-year PM10 mean levels.
Differences in the relationship between DVT risk and PM10 level according to the characteristics of the study subjects are summarized in Table 4. The association between PM10 level and DVT was significantly attenuated in female subjects (P = .02 for the interaction between PM10 level and sex). An increase of 10 µg/m3 in PM10 level was associated with an adjusted OR for DVT of 2.07 (95% CI, 1.50 to 2.84) (P < .001) in men and 1.40 (95% CI, 1.02 to 1.92) (P = .04) in women. No PM10 effect was observed in women taking oral contraceptives or hormone therapy (OR, 0.97; 95% CI, 0.58 to 1.61) (P = .89 for PM10 effect; P = .048 for the interaction between PM10 and hormone use). The other characteristics evaluated, including year of diagnosis, did not significantly modify the association between PM10 exposure and DVT risk (Table 4).

View this table:
[in this window]
[in a new window]
[as a PowerPoint slide]
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

We repeated all the analyses after excluding cases with a recurrent (nonfirst) episode of DVT (n = 110). Risk estimates were very similar to those for the entire study population. Each increase of 10 µg/m3 in PM10 level was associated with an OR of 1.67 (95% CI, 1.27 to 2.22) (P < .001), adjusting for multiple variables. In the subsample of 760 cases with a single episode of DVT, the variations in the association between PM10 level and the risk of DVT due to demographic characteristics, presence of thrombophilia, or use of hormone therapies were similar to those observed in the entire study population.
To evaluate the influence of splines selection in fitting nonliner terms in the logistic models, we repeated all statistical analyses by using natural splines instead of penalized splines. The use of natural splines did not modify the statistical significance of the results, with only small changes in the risk estimates.
We also evaluated the influence of different methods for adjusting for long-term time trends during the study period (supplementary Table 2; available at: As was shown in the subsection "Particle Exposure and Relative Risk of DVT," ignoring long-term time trends in the analyses would have almost completely obscured the association between PM10 level and DVT risk. However, all of the methods for adjustment for long-term time trends that we evaluated in our sensitivity analysis (fitting dummy variables for each year of the study period, as well as linear terms or penalized splines for index date with degrees of freedom varying between 2 and 8) produced risk estimates indicating a significant association between PM10 level and DVT risk, with only small changes due to different handling of the time trends for most of the methods. However, it is worth noting that using only a linear variable for the long-term trend would have produced a lower OR, likely reflecting less than optimal fitting of the time relationships present in our data.


 Jump to Section
 •Author information

In this study of DVT cases and healthy controls, exposure to increased concentrations of particulate air pollution in the year before diagnosis was associated with increased DVT risk after controlling for clinical and environmental covariates. Mean level of PM10 before the examination was also correlated with shorter PT in both cases and controls. The DVT risk increase associated with PM10 level was smaller in women and limited to those who were not using oral contraceptives or hormone therapy at the time of diagnosis.
Long-term exposure to particulate air pollution has been associated with increased risk of coronary heart and cerebrovascular disease in multiple investigations conducted in several countries.4 A systemic increase in thrombotic tendency, secondary to the induction of inflammatory mediators produced in the lungs and released in the circulation or to the translocation of particles of smaller diameter from the lungs into the circulation6 has been frequently proposed to account for the cardiac and cerebrovascular effects of particulate air pollution. In contrast, venous thrombosis has received little attention in studies on the cardiovascular outcomes of air pollution. In a time-series analysis from the Netherlands, Hoek et al16 reported an association of short-term exposure to ambient ozone and, to a lesser extent, black smoke and PM10, with increased mortality from embolism and thrombosis, a broad category that included arterial and venous thromboses in various sites. To date, no study has specifically addressed the association between particulate air pollution and DVT. In our population, we estimated an overall 70% increase in DVT risk with each increase of 10 µg/m3 in PM10 level during the year before diagnosis. For comparison, in the Harvard Six Cities Study, the risk of death from cardiopulmonary diseases was 37% higher in the most polluted compared with the least polluted cities.1 In the Women’s Health Initiative Study, an increase of 10 µg/m3 of annual mean concentrations of PM2.5, which is considered a stronger predictor than PM10 level of air pollution effects, was associated with a 24% increase in the risk of cardiovascular events and a 76% increase in the risk of death from cardiovascular disease.2 The estimated increase in risk of death from all cardiovascular causes associated with 10 µg/m3 elevation in long-term PM2.5 level was 19% in the Harvard Six Cities study and 13% in the study by the American Cancer Society.3
In the present study, PM10 exposure did not increase the risk of DVT in women as much as in men. By evaluating additional risk factors, we found that part—if not all—of such risk attenuation was due to the lack of association between PM10 level and the risk of DVT among women using oral contraceptives or hormone therapy. Such hormone therapies are independent risk factors for DVT,10 which is also confirmed in this study by the higher prevalence of oral contraceptive and hormone use in the cases compared with the controls. Use of oral contraceptives and 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 and reduced levels of the anticoagulant proteins antithrombin and protein S,13, 17-18 that are similar in characteristics and degree to the coagulation changes observed after exposure to air particles.7-8,19-22 We surmise that prothrombotic mechanisms are already activated in those receiving hormone therapy so that they undergo less or no further induction after air particle exposure.
In our analyses, we evaluated DVT risk in association with the level of PM10 measured during the year before diagnosis. In this study, the use of short-term (hourly or daily) air pollution levels would not have been appropriate because DVT presentation is often subtle and its diagnosis has been shown to lag as long as 4 weeks after the initial DVT symptoms.23 In the present work, we demonstrated that mean PM10 level in the year before the examination was associated with shortened PT, extending our previous observation of an association with shorter exposure time windows.13 Interestingly, while the negative effects of mean PM10 levels on PT were independent of the time-window selected, the 1-year mean PM10 was the only exposure metric significantly associated with shortened PT among the cases. In addition, while in our previous work we could not find any relation between 30-day mean PM10 level and aPTT, in our present study, a nonsignificant (P = .07) association was observed between aPTT shortening and 1-year mean PM10 among the controls. This association, taken together with the similar PT change, suggests that 1-year PM10 exposure may also affect aPTT. Thus, the use of PM10 level in the year before diagnosis appeared to capture a fuller range of prothrombotic effects, while also reducing the risks of confounding by seasonal patterns and ambient temperature. This study has the advantage of being based on a large number of DVT cases and controls recruited using a standardized protocol over a long time span. Cases had objective diagnoses of DVT, and both cases and controls were well characterized for inherited and acquired risk factors for DVT. In the statistical analysis, we used models that included nonlinear regression terms to adjust for long-term time trends and day of the year (thus controlling for confounding from year of the study and seasonal variations), in addition to age, sex, area of residence, education, factor V Leiden, G20210A prothrombin mutation, use of oral contraceptive or hormone therapy, body mass index, and ambient temperature.
Because the healthy controls were selected among nonblood relatives and friends of the DVT cases, they tended to be distributed in the 9 study areas, with proportions that were very similar to those of the DVT cases. This might have generated overmatching in our study, ie, the exposure levels of controls may have been more similar to those of DVT cases than they actually are in the population at risk. Therefore, it is possible that risk estimates were underestimated in our study. A limitation of this study is that we used ambient air pollution estimated at the subjects' address as a surrogate for personal exposure, which may have resulted in measurement error, since most subjects conduct a large part of their daily activities away from their residence. A detailed questionnaire was used to ascertain known risk factors for DVT, but no information was collected concerning daily activities, such as time spent outside or in traffic, that could have refined the assessment of PM10 exposure. In addition, our exposure assessment was done by dividing the Lombardy region into 9 areas for which mean PM10 levels were assigned by averaging measurements from multiple monitors. Although these areas were selected to group together territories with similar population densities and geographical characteristics, thus likely reducing within-area variations of the exposure, we were not able to obtain PM10 level estimates at a smaller scale. However, PM10 levels tend to be spatially homogeneous, and a recent study comparing personal exposures with site monitoring in Boston, Massachusetts, reported that monitor readings and personal exposure are highly correlated.24 In addition, it has been shown that using ambient measures to estimate individual exposure is likely to produce an underestimation of pollution effects25 rather than causing the increased risk of DVT found in our study population.
In conclusion, this study provides evidence in support of an association of exposure to particulate air pollution with enhanced prothrombotic mechanisms and risk of DVT. Given the magnitude of the observed effects and the widespread diffusion of particulate pollutants, our findings introduce a novel and common risk factor into the pathogenesis of DVT and, at the same time, give further substance to the call for tighter standards and continued efforts aimed at reducing the impact of urban air pollutants on human health.


 Jump to Section
 •Author information

Correspondence: Andrea Baccarelli, MD, PhD, Exposure, Epidemiology, and Risk Program, Harvard School of Public Health, 401 Park Dr, Landmark Center, Ste 415G W, PO Box 15698, Boston, MA 02215 ( ).
Accepted for Publication: December 14, 2007.
Author Contributions: Study concept and design: Baccarelli, Martinelli, Bertazzi, Mannucci, and Schwartz. Acquisition of data: Baccarelli, Martinelli, Zanobetti, and Grillo. Analysis and interpretation of data: Baccarelli, Martinelli, Zanobetti, Grillo, Hou, Bertazzi, and Schwartz. Drafting of the manuscript: Baccarelli, Hou, Mannucci, and Schwartz. Critical revision of the 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 R83241601 and R827353 from the Environmental Protection Agency Particulate Matter Center; grants ES0002 and ES015172-01 and grant PO1 ES009825 from the National Institute of Environmental Health Sciences; grant 2004-2006/97-C from the MIUR (Ministero dell'Istruzione, dell'Università e della Ricerca) Internationalization Program; and grants UniMi 8614/2006 and UniMi 9167/2007 from theCARIPLO (Cassa di Risparmio delle Provincie Lombarde) Foundation and Lombardy region.
Additional Contributions: Guido Lanzani, PhD, Nadia Carfagno, BSPH, and Anna Cazzullo, MS, ARPA Lombardia, provided support in air-monitoring data handling; and Steve Melly, MS, Harvard School of Public Health, assisted in the creation of geographic maps.
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).


 Jump to Section
 •Author information

1. Dockery DW, Pope CA III, Xu X; et al. An association between air pollution and mortality in six US cities. N Engl J Med. 1993;329(24):1753-1759. FREE FULL TEXT

2. Miller KA, Siscovick DS, Sheppard L; et al. Long-term exposure to air pollution and incidence of cardiovascular events in women. N Engl J Med. 2007;356(5):447-458. FREE FULL TEXT

3. Pope CA III, Burnett RT, Thun MJ; et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA. 2002;287(9):1132-1141. FREE FULL TEXT

4. Brook RD, Franklin B, Cascio W; et al. Air pollution and cardiovascular disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association. Circulation. 2004;109(21):2655-2671. FREE FULL TEXT

5. Utell MJ, Frampton MW, Zareba W, Devlin RB, Cascio WE. Cardiovascular effects associated with air pollution: potential mechanisms and methods of testing. Inhal Toxicol. 2002;14(12):1231-1247. FULL TEXT | ISI | PUBMED

6. Nemmar A, Hoylaerts MF, Nemery B. Effects of particulate air pollution on hemostasis. Clin Occup Environ Med. 2006;5(4):865-881. PUBMED

7. Rückerl R, Ibald-Mulli A, Koenig W; et al. Air pollution and markers of inflammation and coagulation in patients with coronary heart disease. Am J Respir Crit Care Med. 2006;173(4):432-441. FREE FULL TEXT

8. Baccarelli A, Zanobetti A, Martinelli I; et al. Effects of exposure to air pollution on blood coagulation. J Thromb Haemost. 2007;5(2):252-260. FULL TEXT | ISI | PUBMED

9. Lowe GD. Arterial disease and venous thrombosis: are they related, and if so, what should we do about it? J Thromb Haemost. 2006;4(9):1882-1885. FULL TEXT | ISI | PUBMED

10. Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet. 1999;353(9159):1167-1173. FULL TEXT | ISI | PUBMED

11. Vandenbroucke JP, Rosing J, Bloemenkamp KW; et al. Oral contraceptives and the risk of venous thrombosis. N Engl J Med. 2001;344(20):1527-1535. FREE FULL TEXT

12. Silva VM, Corson N, Elder A, Oberdorster G. The rat ear vein model for investigating in vivo thrombogenicity of ultrafine particles (UFP). Toxicol Sci. 2005;85(2):983-989. FREE FULL TEXT

13. van Rooijen M, Silveira A, Thomassen S; et al. Rapid activation of haemostasis after hormonal emergency contraception. Thromb Haemost. 2007;97(1):15-20. ISI | PUBMED

14. Baccarelli A, Zanobetti A, Martinelli I; et al. Air pollution, smoking, and plasma homocysteine. Environ Health Perspect. 2007;115(2):176-181. ISI | PUBMED

15. Wood SN. Modelling and smoothing parameter estimation with multiple quadratic splines. J R Stat Soc Ser B Methodological. 2000;62(1):95-114.

16. Hoek G, Brunekreef B, Fischer P, van Wijnen J. The association between air pollution and heart failure, arrhythmia, embolism, thrombosis, and other cardiovascular causes of death in a time series study. Epidemiology. 2001;12(3):355-357. FULL TEXT | ISI | PUBMED

17. Rosendaal FR, Van Hylckama Vlieg A, Tanis BC, Helmerhorst FM. Estrogens, progestogens and thrombosis. J Thromb Haemost. 2003;1(7):1371-1380. FULL TEXT | ISI | PUBMED

18. Rabbani LE, Seminario NA, Sciacca RR, Chen HJ, Giardina EG. Oral conjugated equine estrogen increases plasma von Willebrand factor in postmenopausal women. J Am Coll Cardiol. 2002;40(11):1991-1999. FREE FULL TEXT

19. Schwartz J. Air pollution and blood markers of cardiovascular risk. Environ Health Perspect. 2001;109(suppl 3):405-409. FULL TEXT | ISI | PUBMED

20. Ghio AJ, Hall A, Bassett MA, Cascio WE, Devlin RB. Exposure to concentrated ambient air particles alters hematologic indices in humans. Inhal Toxicol. 2003;15(14):1465-1478. ISI | PUBMED

21. Riediker M, Cascio WE, Griggs TR; et al. Particulate matter exposure in cars is associated with cardiovascular effects in healthy young men. Am J Respir Crit Care Med. 2004;169(8):934-940. FREE FULL TEXT

22. Liao D, Heiss G, Chinchilli VM; et al. Association of criteria pollutants with plasma hemostatic/inflammatory markers: a population-based study. J Expo Anal Environ Epidemiol. 2005;15(4):319-328. FULL TEXT | ISI | PUBMED

23. Elliott CG, Goldhaber SZ, Jensen RL. Delays in diagnosis of deep vein thrombosis and pulmonary embolism. Chest. 2005;128(5):3372-3376. FULL TEXT | ISI | PUBMED

24. Sarnat JA, Brown KW, Schwartz J, Coull BA, Koutrakis P. Ambient gas concentrations and personal particulate matter exposures: implications for studying the health effects of particles. Epidemiology. 2005;16(3):385-395. FULL TEXT | ISI | PUBMED

25. Zeger SL, Thomas D, Dominici F; et al. Exposure measurement error in time-series studies of air pollution: concepts and consequences. Environ Health Perspect. 2000;108(5):419-426. ISI | PUBMED

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

Particulate Air Pollution Exposure and Risk of Venous Thromboembolism
James E. Dalen
Arch Intern Med. 2008;168(22):2497.


Potential Health Risks of Air Pollution Beyond Triggering Acute Cardiopulmonary Events
Robert D. Brook
JAMA. 2008;299(18):2194-2196.

Air Pollution: What Is Bad for the Arteries Might Be Bad for the Veins
Robert D. Brook
Arch Intern Med. 2008;168(9):909-911.


Living Near Major Traffic Roads and Risk of Deep Vein Thrombosis
Baccarelli et al.
Circulation 2009;119:3118-3124.

The Expanding Role of Air Pollution in Cardiovascular Disease: Does Air Pollution Contribute to Risk of Deep Vein Thrombosis?
Circulation 2009;119:3050-3052.

Breathe Deeply into Your Genes!: Genetic Variants and Air Pollution Effects
Am. J. Respir. Crit. Care Med. 2009;179:431-432.

Climate change and health costs of air emissions from biofuels and gasoline
Hill et al.
Proc. Natl. Acad. Sci. USA 2009;106:2077-2082.

Particulate Air Pollution Exposure and Risk of Venous Thromboembolism
Arch Intern Med 2008;168:2497-2497.

Particulate Air Pollution and DVT Risk
JWatch General 2008;2008:4-4.

All you need to read in the other general journals
BMJ 2008;336:1156-1157.

Potential health risks of air pollution beyond triggering acute cardiopulmonary events.
JAMA 2008;299:2194-2196.

Air Pollution: What Is Bad for the Arteries Might Be Bad for the Veins
Arch Intern Med 2008;168:909-911.


© 2008 American Medical Association. All Rights Reserved.