Superfund Research Program

Analysis of PAHs in Air Samples Collected After the WTC Disaster and Estimation of Increase in Lifetime Cancer Risk

Release Date: 09/01/2004

The collapse of the World Trade Center (WTC) on September 11, 2001 released an estimated 1 million tons of dust and smoke into the air of New York City (NYC). More than 90% of the airborne mass consisted of particles of pulverized concrete, metals, silica, and organic materials that were larger than 10 µm in diameter. Because large particles do not penetrate deeply into the lungs, the vast majority of the dust generated by the collapse of the WTC posed a relatively small health risk to the general public. These large alkaline particles were irritating to the upper airways of exposed individuals, but settled quickly from the air. However, fine particulate matter (particles with diameter <2.5 µm, PM2.5) was continually emitted from Ground Zero during the cleanup, and was widely dispersed throughout greater NYC. Estimates based on the settled dust suggest that 11,000 tons of PM2.5 were released. Given their deep penetration into the lungs, PM2.5 particles represent great potential risk to the public health.

The PM2.5 fraction contained materials from the pulverized WTC structures and soot particles from fires that persisted from September 11 through December 20, 2001. The soot contained numerous carcinogens, notably polycyclic aromatic hydrocarbons (PAHs), which are ubiquitous products of incomplete combustion. PAHs have frequently been associated with human cancers of the skin, lungs, and bladder, as well as with elevated levels of DNA adducts and P53 mutations in humans. Airborne PAHs have also been implicated in human reproductive effects.

Following the WTC disaster, the U.S. Environmental Protection Agency (EPA) collected air samples at or near Ground Zero to monitor a variety of pollutants, and deployed monitors for PM2.5 at four locations. Samples were collected daily using Teflon filters at each site (~24-hour duration) between September 23, 2001 and March 27, 2002. After performing nondestructive assays for particle mass and metal content, the EPA archived the Teflon filters.

Dr. Stephen Rappaport of the University of North Carolina-Chapel Hill SBRP, working with EPA scientists led by Joachim Pleil, developed an analytical method for assaying particle-bound PAHs in archived Teflon PM2.5 filters. The method employs solvent extraction followed by concentration and analysis by gas chromatography-mass spectrometry (GC-MS) with electron ionization and selective ion monitoring. The researchers evaluated the method for sensitivity, recovery, precision, and agreement of paired air samples and determined that the assessment of particle-bound 5- and 6-ring PAHs from archived PM2.5 filters is quantitatively robust. They found that the assay may also be useful for selected 4-ring compounds, notably chrysene and benzo(a)anthracene, if the PM2.5 filters are stored under refrigeration.

The research team used their new method to measure nine PAHs, including some of the most carcinogenic compounds, in 243 of EPA's archived PM2.5 samples. They observed that the relative contributions of several PAHs changed significantly during the 200-day sampling period, and concluded that PAHs arose from the following three processes after 9/11/2001:

  • PAHs generated by the fires at Ground Zero - these PAHs were continually generated by smoldering fires and exhibited an exponential decline in concentration over time as the available fuel was consumed;
  • PAHs generated by diesel equipment used to clear the rubble from Ground Zero - as cleanup activity progressed, diesel sources diminished from mid-September 2001 to May 28, 2002 and these PAHs exhibited a quasi-linear decline in concentration;
  • PAHs generated by background sources of diesel exhaust, including trucks and buses, that existed in NYC during and after cleanup activities at the WTC site - emission rates for these PAHs remained constant during the sampling period.

Having identified these processes, the researchers constructed a statistical model to characterize PAH levels in the samples. Their results indicate that, in the immediate aftermath of the WTC disaster, PAH concentrations at Ground Zero were 10- to 214-fold greater than background values (median = 58 fold). However, air levels rapidly declined with the dissipation of fires during the first 100 days (with a half life of 14.5 days), and slowly declined thereafter as diesel equipment was phased out.

Given the rapid decline of PAH levels in the aftermath of September 11, 2001, Rappaport and his colleagues consider it unlikely that the long-term risks of cancer arising from PAHs would have been significantly elevated above those from background PAH exposures in NYC over 70 years. Indeed, employing standard methods, they estimate only a 10-8 increase in lifetime cancer risk at Ground Zero from WTC-related PAHs. However, they state that their conclusion regarding cancer risks from PAHs cannot be extended to other carcinogenic substances that were also released to the air after the WTC disaster.

The researchers are careful to note that their conclusion about low lifetime cancer risks should not be interpreted to mean that there are no health risks in the population exposed to PAHs. In particular they mention the following subpopulations that might be at particular risk:

  • Workers engaged in the cleanup efforts could have been exposed to much higher levels of PAHs than those measured in the EPA air samples (collected at the perimeter of Ground Zero).
  • The offspring of women who were (or became) pregnant during the weeks following September 11, 2001 may be at risk because the high PAH levels in the immediate aftermath of the disaster present the potential for adverse reproductive effects. Recent studies suggest that the fetus may be at particular risk to PAH damage and preliminary results of another SBRP-funded study point to a 2-fold elevation of intrauterine growth restriction among the offspring of women residing close to the WTC during the weeks after September 11 (See: JAMA 290(5):595-596). By carefully mapping PAH levels in space and time after the WTC disaster, it may be possible to determine the nature and extent of links between PAH exposure and developmental effects in the local population.

The researchers also caution that the transient nature of exposures to high levels of PAHs from the WTC disaster is only indicative of outdoor air, where massive dilution rapidly reduced the air concentrations. However, dust and soot from the WTC disaster also deeply penetrated residential and commercial buildings, leaving thick layers of residue. Human indoor activities and contaminated central ventilation, heating, and cooling systems can continually resuspend settled dusts into the air; therefore, indoor air may represent a continuing source of exposure to PAHs (and other particle-related pollutants) that should be considered.

Because no PAH-specific air sampling was conducted in the community following the WTC disaster, this work provides the only systematic measurements, to our knowledge, of ambient PAHs following September 11, 2001.

For More Information Contact:

Stephen M Rappaport
University of California-Berkeley
School of Public Health, Department of Environmental Health Sciences
2121 Berkeley Way West, Room 5302
Berkeley, California 94720-7360
Phone: 510-642-4355

To learn more about this research, please refer to the following sources:

  • Pleil JD, Vette AF, Johnson BA, Rappaport SM. 2004. Air levels of carcinogenic polycyclic aromatic hydrocarbons after the World Trade Center disaster. Proc Natl Acad Sci U S A 101(32):11685-11688. PMID:15280534
  • Pleil JD, Vette AF, Johnson BA, Rappaport SM. 2004. Assaying particle-bound polycyclic aromatic hydrocarbons from archived PM2.5 filters. J Chromatogr A 1033(1):9-17. PMID:15072286

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