Bring the Green Line to Somerville

(Mass. DEP, submitted 1/17/06)

January 17, 2006

Ms Christine Kirby
Department of Environmental Protection
Bureau of Waste Prevention
One Winter Street, 10th Floor
Boston, MA 02108
christine.kirby@state.ma.us

Dear Ms. Kirby:

This letter is to reiterate my support for the changes to the Ozone SIP needed to allow the extension of the Green Line through Somerville's Union Square into Medford Hillside. I wish to thank the Commonwealth for its current support for this project, which has been discussed but never implemented for over forty years. I also, however, wish the Commonwealth to reconsider dropping the restoration of the Arborway Green Line to Jamaica Plain and also the connection of the Red and Blue Lines. Both of these are very worthwhile projects that will do a great deal to keep the citizens of affected areas out of their automobiles. Jamaica Plain, in particular, counts as an Environmental Justice area that, like Somerville, should not bear an undue burden of the environmental costs of regional transportation.

Somerville has a large proportion of disadvantaged populations, especially around I-93 and Routes 28 and 38 in East Somerville. For decades, Somerville has paid the environmental costs of transportation services that primarily benefit other people. More commuters now travel through or close to East Somerville than in any other Boston corridor. I-93 and Routes 28 and 38 carry 250,000 vehicles per day. Local collectors that connect to these highways add out-of-town commuters and shoppers to swell local traffic volumes. Six passenger rail lines cut through Somerville without stopping, carrying two hundred highly-polluting diesel trains per day. Somerville pays as much in MBTA assessment as cities with three to five T-Stops, yet Somerville has only one T-Stop of its own, in Davis Square at the edge of West Somerville.

Before I-93 was completed in the early 1970's, DEP learned that Somerville would go into violation of the Clean Air Act as a result. The Commonwealth went ahead anyway without mitigating those impacts. Finkelstein et al (2005) has shown that there is an association between living in a disadvantaged neighborhood exposed to increased levels of ambient particulate matter, gaseous pollutants, and traffic, and increased incidence of coronary heart disease, even taking socioeconomic factors into account.

Environmental justice can only be attained if low-income, minority, and immigrant populations get their fair share of transportation benefits and not suffer an unfair share of its costs. Please place environmental justice considerations high on your list of criteria for updating the Ozone SIP, both for Somerville and Jamaica Plain.

DEP should, by policy, evaluate the public-health consequences of all transportation projects, and particularly those in vulnerable areas such as East Somerville. Somerville, which lies next to Interstate 93, Route 28, Route 38, and other major thoroughfares, leads the state in excess lung cancer and heart attack deaths per square mile per year. Somerville residents smoke less than the state average, yet Massachusetts public health records from 1996-2000 show 29 excess deaths per year over five years in Somerville, even adjusted for population density and age.

Children who grow up in heavily polluted areas like East Somerville are four times as likely never to achieve full lung capacity as are those who grow up in cleaner areas.
Fine particulate matter produced by automobiles and other mobile sources penetrates deep into the lungs and inflames cardiovascular systems. It causes both lung diseases and heart disease. Recent Federal EPA studies show a linear relationship between air pollution and excess deaths from lung cancer and heart attacks. People living within 100 meters of a freeway and within 50 meters of other major roadways are much more likely to die from heart and lung diseases than are people who live farther away. Nyberg et al. (2000) has shown that average traffic-related NO2 exposure over 30 years was associated with an increased risk of lung cancer among stable residents of Stockholm. Gauderman et al (2005) has shown that lifetime history of doctor-diagnosed childhood asthma was associated with measures of outdoor nitrogen dioxide (NO2) outside the home of each child, and that increased asthma was associated with closer residential distance to a freeway and with estimates of pollution from a freeway. Perera et al. showed that the developing fetus is more susceptible than the mother to the carcinogenic effects of polycyclic aromatic hydrocarbons released by transportation vehicles, power generation, and other combustion sources.

DEP should not content itself with using its regulatory power to make improvements in regional pollution measures, but should actively promote projects that mitigate the public health consequences of environmental hot spots such as occur in East Somerville. Health effects are local, associated with "hot spots" downwind of major pollution sources like I-93 and other arterial highways. These local hot spots can be averaged away by more remote, suburban areas. For instance, Knox (2005) has shown that childhood cancers were strongly determined by prenatal exposures to oil-based combustion gases, especially from engine exhaust, and strongly reinforced when associated with bus stations, hospitals, railways, oil installations, and other local hot spots. Jerrett et al. (2005) has shown that chronic health effects due to ischemic heart disease and lung cancer associated with small area exposures are nearly 3 times larger than when measured between communities. As noted above, Gauderman et al. (2005) has shown that increased asthma was associated with closer residential distance to a freeway and with estimates of pollution from a freeway.

I wish to make one final point. It was apparent from the January 17, 2006 Boston Globe article "Big Gaps in State Plans for Emissions" that the current emissions plans focus on power plants and similar facilities, rather than on vehicular sources of air pollution,. This is a huge policy omission, since a major part of the total pollution burden, including greenhouse gases, comes from vehicles. DEP should rectify this omission as soon as possible.

Thank you for your attention.

Sincerely,

David Dahlbacka
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References:

Finkelstein, Murray M.; Jerrett, Michael; and Sears, Malcolm R. "Environmental inequality and circulatory disease mortality gradients." J. Epidemiological Community Health. 59:481-487, 2005.

This study examined the association between living in a disadvantaged neighborhood and increased incidence of coronary heart disease. Subjects in more deprived neighborhoods were more exposed to ambient particulate pollutants, gaseous pollutants, and to traffic, and had higher mortality due to circulatory disease than subjects in less deprived neighborhoods, even taking socioeconomic factors into account.

Gauderman, W. James; Avol, Edward; Lurmann, Fred; Kuenzli, Nino; Gilliland, Frank; Peters, John; and McConnell, Rob. "Childhood Asthma and Exposure to Traffic and Nitrogen Dioxide." Epidemiology. 16:6, November 2005.

This study examined the association between traffic-related pollution and childhood asthma. Lifetime history of doctor-diagnosed asthma was associated with measures of outdoor nitrogen dioxide (NO2) outside the home of each child. Increased asthma was associated with closer residential distance to a freeway and with estimates of pollution from a freeway.

Jerrett, Michael; Burnett, Richard T.; Ma, Renjun; Pope, C. Arden III; Krewski, Daniel; Newbold, K. Bruce; Thurston, George; Shi, Yuanli; Finkelstein, Norm; Calle, Eugenia E.; and Thun, Micheal J. "Spatial Analysis of Air Pollution and Mortality in Los Angeles." Epidemiology. 16:6, November 2005.

This study compared the assessment of exposure to ozone and fine particulate matter air pollution using community average concentrations with that using small-area exposure measures. The results suggested that chronic health effects due to ischemic heart disease and lung cancer associated with small-area exposures are nearly 3 times larger than when measured between communities. Fine particulate matter was associated more strongly with ischemic heart disease than with cardiopulmonary mortality or mortality from all causes.

Knox, E.G. "Oil combustion and childhood cancers." J. Epidemiological Community Health. 59:755-760, 2005.

This study examined the risks of child deaths from cancer near hotspots from carbon monoxide, PM10 particles, nitrogen oxides, 1,3-butadiene, benzene, dioxins, benzo(a)pyrene, and volatiles. The conclusions were that childhood cancers are strongly determined by prenatal or early postnatal exposures to oil based combustion gases, especially from engine exhausts. 1,3-butadiene (a known carcinogen) and carbon monoxide were powerful independent predictors of childhood cancer, strongly reinforced when associated with bus stations, hospitals, railways, oil installations, and industrial transport centers.

Nyberg, Fredrik; Gustavsson, Per; Jaerup, Lars; Bellander, Tom; Berglind, Niklas; Jakobsson, Robert; and Pershagen, Goeran. "Urban Air Pollution and Lung Cancer in Stockholm." Epidemiology. 11:5, September 2000.

This 30-year retrospective study dealt with lung cancer among stable residents of Stockholm in association with NOx and SO2. Average traffic-related NO2 exposure over 30 years was associated with an increased risk of lung cancer after a latency period of 20 years.

Perera, Frederica P.; Tang, Deliang; Tu, Yi-Hsuan; Cruz, Linda Ali; Borjas, Mejico; Bernert, Tom; and Whyatt, Robin M. "Biomarkers in Maternal and Newborn Blood Indicate Heightened Fetal Susceptibility to Procarcinogenic DNA Damage". Environmental Health Perspectives. 112:101, July 2004.

This article reported that the developing fetus is more susceptible than the mother to the carcinogenic effects of polycyclic aromatic hydrocarbons (PAHs) such as benzo(a)pyrene (BaP) released by transportation vehicles, power generation, and other combustion sources. Although the estimated dose reaching the fetus is one tenth that reaching the mother, mean levels of BaP cancer biomarkers were comparable between newborns and their mothers.

18-Feb-2007