June 13, 2001Ê



Ms. Helene Goldberger
Administrative Law Judge
DEC Office of Hearings & Mediation Services
50 Wolf Road
Albany NY 12233-1550Ê


Dear Judge Goldberger:Ê

Thank you for your prompt response to my letter of May 22 and for your recent extension of the period for filing for status. As I am neither a lawyer nor sufficiently wealthy, I regret that I will not be able to apply for party status. However, I will try to express in this letter the concerns which I would have stated at a hearing. They are for the health of our community and, I believe, are addressed by the Declaration of Policy and other statutes of the Environmental Law of New York State.Ê

As you may recall, I am a Board Certified pediatrician who has practiced pediatrics in Columbia County since 1964. For many of those years I was Chief of Pediatrics at Columbia Memorial Hospital and an Associate Clinical Professor of Pediatrics at Albany Medical School. Although I no longer practice full-time, I continue to see patients three or four mornings a week and keep abreast of the current medical literature.Ê

My interest in the new cement plant began after reading the material in the ÒHandbook of Pediatric Environmental HealthÓ recently published by the American Academy of Pediatrics. The book states: ÒIn children, acute health effects associated with outdoor air pollution include increased respiratory symptoms, such as wheezing and cough, transient decrements in lung function, more serious lower respiratory tract infections, and exacerbations of asthma.Ó1Ê

I contacted the editor of the handbook, Ruth A. Etzel, M.D. Ph.D., and obtained additional references so that I could see for myself the sources upon which this statement was based. My readings, combined with my review of the Draft Environmental Impact Statement (DEIS) submitted by St. Lawrence Cement (SLC), gave me great concern regarding the health consequences to our community once the plant begins operation.Ê

 My greatest worry involves the particulate matter which will be released by the total process involved in the production of cement. The suggested National Ambient Air Quality Standards (NAAQS) for PM10 (Particulate Matter smaller than 10 microns) and PM2.5 (smaller than 2.5 microns) are:Ê

	pollutant	ÊÊÊÊÊambient air limit averaging timeÊ

	PM10	50 ug/m3	ÊÊÊÊannual arithmetic mean/24 hoursÊ	150 ug/m3	ÊÊÊÊÊmaximum/24 hoursÊ

	PM2.5	15ug/m3	Ê	Êannual arithmetic mean/24 hourÊ	ÊÊÊ50 ug/m3	ÊÊÊÊÊmaximum/24 hoursÊ

However, these standards are inadequate to protect the health of many children and adults suffering with pulmonary or heart problems. I emphasize this last well-established scientific fact because I believe it must be considered before issuing any permit for the construction of this plant.Ê

In an article published in the December 14, 2000 issue of The New England Journal of Medicine (one of the most prestigious medical journals in the world) entitled ÒFine Particulate Air Pollution and Mortality in 20 U.S. Cities, 1987-94Ó,2 the authors state in the abstract of their results: ÒThe estimated increase in the rate of death from cardiovascular and respiratory causes was 0.68% for each increase in PM10 level of 10 micrograms per cubic meter.Ó This figure negates the NAAQS; the death rate went up with each increase of 10 micrograms per cubic meter whether the ambient air level of PM10 was initially 20 or 40 or 120, all levels within published ÒacceptableÓ standards.Ê

There are many other articles in the medical literature corroborating the shortcomings of our present standards. I will mention a few.Ê

Peters et al. in their article, ÒAir Pollution and Incidence of Cardiac ArrythmiaÓ,3 demonstrate a linear progression of defibrillator discharges (indicating cardiac arrythmias) for susceptible individuals as the PM2.5 rises from 5 micrograms/meter cubed to 25 micrograms/meter cubed. (Italics mine.) This effect occurred after a two-day lag period. Again, pollution levels were all within established acceptable limits. 

In their article, ÒAn Association between Fine Particles and Asthma Emergency Department Visits for Children in SeattleÓ4, Norris et al. state in their introductory abstract: ÒSignificant associations were found between ED visits for asthma in children and fine PM and CO.Ó Importantly, they continue, ÒThese findings were seen when estimated PM2.5 concentrations were below the newly adopted annual National Ambient Air Quality Standard of 15 micrograms/meter cubed.ÓÊ

 Schwartz and associates, in their article, ÒAcute Effects of Summer Air Pollution on Respiratory Symptom Reporting in ChildrenÓ5, indicate that ÒA change in 24-h PM10 concentration from 20 to 50 micrograms/meter cubed was associated with relative odds of 1.53 for the incidence of lower respiratory symptoms, a relative odds of 1.22 for the incidence of coughing, and a relative odds of 1.22 for the incidence of upper respiratory symptoms.Ó They also note, and I would again wish to emphasize this, ÒThe highest daily PM10 concentration was 117 micrograms/meter cubed during the study, indication that these relationships occurred at concentrations below the ambient air quality standard.ÓÊ

In their paper, ÒAcute Effects of Ambient Air Particles in Asthmatic and Nonasthmatic Children6, Vedal et. al. report: ÒIt is concluded that children experience reductions in Pulmonary Expiratory Flow and increased symptoms after increases in relatively low ambient PM10 concentrations, and that children with diagnosed asthma are more susceptible to these effects than are other children.ÓÊ

It is also important to note the study published by Woodruff and colleagues entitled ÒThe Relationship between Selected Causes of Postneonatal Infant Mortality and Particulate Air Pollution in the United StatesÓ7. The authors state in their abstract: ÒOverall postneonatal mortality rates were 3.1 among infants with low PM10 exposures, 3.5 among infants with medium PM10 exposures and 3.7 among highly exposed infants. After adjustment for other covariates, the odds ratio (OR) . . . for total postneonatal mortality for the high exposure versus the low exposure group was 1.10. In normal birth weight infants, high PM10 exposure was associated with respiratory causes (OR=1.40) and sudden infant death syndrome (OR=1.26).Ó The ambient air levels involved were two-month averages following the births studied. The ÒlowÓ category was a PM10 of 23.6 ug/m3 (range 11.9-28.0), the ÒhighÓ, 44.5ug/m3 (range 40.01-68.8), all within the regulatory standard.Ê

The above are only samples of the many reports in the peer-reviewed medical literature substantiating that Particulate Matter is dangerous to public health at levels well below NAAQS, the same standards used by the New York State Department of Environmental Conservation when evaluating any DEIS. This despite the fact the DEC is responsible under NY State legislation to protect the health of its citizens.Ê

Let us now turn to the SLC DEIS and the information it contains regarding particulate matter, keeping in mind the knowledge gained from the above (and similar) reports.Ê

In Table C-17 on page C-34 of the SLC Air Permit Application portion of the DEIS, the average annual daily increase of PM10 is given as 7.38 microgms/m3, raising the ambient air concentation by over 40% to a total of 25.4microgm/m3. The same table indicates the 24 hour maximum might go as high as 49.46, raising the background maximum by almost 50% to a total of 105 microgms/m3. Because the NAAQS for the 24 hour maximum is 150 and that for the annual daily average is 50, the DEIS ÒcompliesÓ despite the latest medical information indicating that levels in this range produce problems in susceptible individuals.Ê

Of additional concern is the information listed in Table C-8 on page C-13 in the same section of the DEIS. The table is entitled Results of Worst Case Modeling Analysis for the Kiln Stack. Here we are informed that the PM10 hourly rate of emission might reach over 18 micrograms/m3 (italics mine). One is left to assume that this scenario can never occur for even three hours since this would bring the daily total above the 49.46, which SLC reports as its maximum in Table C-17. Will this guarantee be in the Permit for the project? Will the local population be warned immediately if the worst case scenario occurs? Or will the physicians of the community just have to guess as to the cause of increased cardiac and respiratory morbidity and mortality in the ensuing few days?2,5,6 Worse still, will anyone even know of the occurrence if it doesnÕt happen on the one in six days the DEC is mandated to check on PM10 levels? The DEIS also includes a section devoted to PM2.5 (Appendix H2: Particulate Matter and PM2.5). The discussion leads off by reporting the difficulties faced in measuring PM2.5 and in being able to interpret the medical data accumulating on this subject. Nevertheless, the conclusion of Appendix H2 knowingly reports Ò . . . it is expected that the proposed project would contribute to a reduction in airborne particulate matter, especially PM2.5Ó.

However, the first sentence of this same concluding paragraph states that the project Òwould result in some small increases in ambient particulate concentrations in the vicinity of the Greenport facilityÓ. And what might these small increases actually be? On page H2-8 the DEIS indicates an occasional daily average of as much as 8 microgm/m3 and rarely up to 11 microgm/m3. Once again, levels that are technically acceptable but demonstrably harmful.3,4 Furthermore, with regard to PM2.5, the DEIS states on page H2-3: The EPA assessment contained in the 1996 Criteria Document focuses on several epidemiology studies that link health effects statistically to concentrations of PM2.5 in ambient air. However, statistical correlations are only one form of evidence as to health effects, and may be plagued by technical flaws such as bias and statistical confounding of multiple pollutants. Further evidence from other types of studies appears to contradict the results of the population-based statistical studies. In particular controlled exposures of individuals (both human and laboratory animals) to ambient concentrations of fine particulate matter failed to invoke symptoms.Ó The authors of the DEIS offer no references to establish this claim. However, one of their consultants, Dr. Laura Green, was kind enough to send me some of the articles which allegedly indicated that controlled exposures of fine particulate matter to individuals did not provoke symptoms in those individuals. In fact, many of the articles had significant scientific weaknesses (such as giving group results without reporting the individual data or testing a group too few in number to yield statistically significant results). Remarkably, in some cases, the studies show just the opposite result of what the DEIS reports as quoted above.Ê

For example, in the article by Hanley, Koenig, Larson, Anderson and associates entitled ÒResponse of Young Asthmatic Patients to Inhaled Sulfuric AcidÓ,8 the abstract admits: ÒSignificant (negative) group responses to FEV1 and FECÓ(lung function tests) Òwere seen measured 2 to 3 minutes post exposure.Ó But then they continue by stressing Òpulmonary function changes 20 minutes postexposure did not show a significant group responseÓ (italics mine). However, if one reads the entire paper and looks at Table 2, it is readily apparent that inhaled sulfuric acid provoked significantly diminished lung function 20 minutes after exposure for at least 5 of the 22 individuals studied. Presumably, in the opinion of the DEIS, producing diminished lung function in over 20% of those studied doesnÕt count. Another reference allegedly showing Òinability to provoke responsesÓ was a paper by Anderson, Avol, Linn, and Hackney, et. al. entitled ÒControlled Exposures of Volunteers to Respirable Carbon and Sulfuric Acid AerosolsÓ,9 published in ÒThe Journal of the Air and Waste Management AssociationÓ in 1992. In a boxed offset area on the first page of the article, the following statement is made: Implications Epidemiologic evidence suggests substantial health risk from acidic ambient particulate pollution but is not strongly supported by human laboratory evidence.

Thus, specific regulation of acidic aerosols remains controversial. This study aimed to resolve the discrepancy through more realistic laboratory exposures, employing acid-coated insoluble respirable particles instead of aqueous aerosol. Exposed volunteers were not affected meaningfully, except for an equivocal response by one individual. Thus the discrepancy between epidemiological and laboratory evidence remains to be resolved. (Italics mine.) Yet, at the end of the same paper the authors in their discussion state that Ò . . . our one atypical subject (see Table IV) might be thought to represent a vulnerable subgroup, and to have experienced real, clinically significant respiratory disturbances from exposure to H2SO4 adsorbed on carbon particles.Ó Nevertheless, in their prominently displayed ÒImplicationsÓ, the authors fail to mention that this one ÒatypicalÓ subject was dropped from the study and her data Òexcluded from group statisticsÓ because her diminished lung function in response to the test was so dramatic that Òthe medical safety officer terminated her exposure.Ó Nor do they note that as there were only 15 subjects involved in the entire study, this ÒatypicalÓ subject comprised 6.67% of the population involved. A third study among the group sent to me, one by Frampton, Morrow, Utell and colleagues entitled ÒSulfuric Acid Aerosol Followed by Ozone Exposure in Healthy and Asthmatic SubjectsÓ,10 states in its abstract: ÒIndividual responses among asthmatic subjects were quite variable, some demonstrating reductions in FEV1 of more than 35% . . . Ó The abstract concludes as follows: ÒAsthmatic subjects differ from healthy volunteers in their functional responses following sequential exposures to aerosols and ozone and appear to represent a susceptible population.Ó Ironically, these papers do not demonstrate a ÒdiscrepancyÓ but rather reinforce exactly what the statistical studies continue to show: a small but significant percentage of susceptible individuals suffer serious health effects from particulate matter. 

If it is appropriate and legal for the DEC to accept a DEIS that makes such unsubstantiated claims regarding the effects of PM2.5, one must wonder about the validity of the other assertions and data reported in the DEIS. Who is checking the ÒfactsÓ presented by SLC? Why are they apparently accepted at face value? The DEC is mandated to protect the public health of the citizens of New York. Is it fulfilling its responsibility? Moreover, despite an eleven-page discourse on PM2.5, the DEIS offers no information on the effects of the increased diesel truck traffic caused by the plant and the consequences of these diesel engine particulate emissions.

In Chapter 13: ÒTraffic and TransportationÓ, there is an extended analysis of the effects on local roads of this increase in truck movement. Page 13-12 reports: ÒSLC estimates that approximately 400,000 metric tons per year (mty) of cement product would be shipped by truck from the Greenport facility each year. For the peak month, this is estimated to result in a maximum of 120 fully enclosed, 25-ton capacity trucks per day. These numbers are expected to be lower during non-peak months, particularly in the winter months. The average daily truck movement is estimated to be 90 vehicles per day (vpd) for cement.Ó

Since it is well known that diesel engines are a significant source of Particulate Matter pollution, why werenÕt these emissions discussed with regard to Air Quality? What will be the effect on the families whose homes are on the truck route during the dog days of August? And what of the added effects (as noted on page 13-13), from the delivery of fly ash to the plant, of by Òup to 25 trucks per dayÓ and of the removal of the cement kiln dust from the plant by Òup to an additional 15 trucks per dayÓ? I believe these are matters that should have definitely been addressed in the DEIS but are not. This serious error of omission has not been questioned by the DEC.Ê

The Consolidated Laws of the State of New York, Chap.43-B, ÒEnvironmental ConservationÓ, in Art. 1, Title 1, Sec. 1-0101 makes a ÒDeclaration of PolicyÓ which includes the followingÊ

 1. The quality of our environment is fundamental to our concern for the quality of life. It is hereby declared to be the policy of the State of New York to conserve, improve and protect its natural resources and environment and control water, land and air pollution, in order to enhance the health, safety and welfare of the people of the state and their overall economic and social well being.Ê

 2. It shall further be the policy of the state to. . .develop and manage the basic resources of water, land, and air to the end that the state may fulfill its responsibility as trustee of the environment for the present and future generations.Ê

 3. It shall further be the policy of the state to foster, promote, create and maintain conditions under which man and nature can thrive in harmony with each other, and achieve social, economic and technological progress for present and future generations by: a. Assuring surroundings which are healthful and aesthetically pleasing; b. Guaranteeing that the widest range of beneficial uses of the environment is attained without risk to health or safety, unnecessary degradation or other undesirable or unintended consequences; c. Promoting patterns of development and technology which minimize adverse impact on the environment; d. Preserving the unique qualities of special resources such as the Adirondack and Catskill forest preserves; e. Providing that care is taken for the air, water and other resources that are shared with the other states of the United States and with Canada in the manner of a good neighbor.Ê

In view of this declared statutory policy (1-0101. 1.) and the known medical consequences of levels of PM less than the accepted NYS DEC standards,2,3,4,5,6,7 how can it be legal to allow this project to go forward? Moreover, considering that SLC believes it will continue mining and producing cement in the area for 100 years or more, how can the present permit, if issued, comply with Sec. 1-1010. 2. regarding those future generations? Both of these questions are particularly pertinent when one considers that in Sec. 1-0101. 3.b., the State is Òguaranteeing that the widest range of beneficial uses of the environment is attained without risk to health and safety . . . Ó Although Sec. 1-0101. 3.c. fosters Òpromoting patterns of development and technology which minimize adverse impact on the environmentÓ, it does not mention health specifically nor does ÒpromotingÓ rise to the level of requirement that ÒguaranteeingÓ implies.Ê

Art. 3, Title 3 outlines the general functions, powers and duties of the department (DEC) and the commissioner. Sec. 3-0301 states:Ê

It shall be the responsibility of the department, in accordance with such existing provisions and limitations as may be elsewhere set forth in law, by and through the commissioner to carry out the environmental policy of the state set forth in section 1-0101 of this chapter.Ê

In view of these statutory responsibilities, what is the legal basis for allowing a project to proceed when neither the commissioner nor the department would be following the policy Òset forth in section 1-0101 of this chapterÓ? They certainly cannot ÒguaranteeÓ that the effects of the plant will be Òwithout risk to health and safetyÓ of the surrounding community, a fact which must be admitted when one combines the data in SLCÕs own DEIS and presently known medical information.Ê

Sec.3-0301 continues:Ê

In so doing the commissioner shall have power to:

* Monitor the environment to afford more effective and efficient control practices, to identify changes and conditions in ecological systems and to warn of emergency conditions;

* To prevent and control air pollution emergencies, as defined in subdivision 1 of section 1-0303 hereof. In exercising such prevention and control the department and the commissioner may limit the consumption of fuels and use of vehicles, curtail or require the cessation of industrial processes and limit or require the cessation of incineration and open burning, and take any other action he may deem necessary to prevent and/or control air pollution emergencies. The department and commissioner shall adopt and implement by rule and regulation a plan designed to prevent and control such air pollution emergencies. Sec. 1-0301, referred to in Sec. 3-0301.y., contains the following definition: 1. "Air pollution emergency" means a combination of circumstances which requires immediate action to reduce the quantity of contaminants in the atmosphere due to danger to public health and welfare, injury to agricultural crops and livestock, damage to and deterioration of property, hazards to air and ground transportation or impairment of environmental quality. Furthermore, in Sec. 8-0103, the legislature finds and declares that: . . . 

* The capacity of the environment is limited, and it is the intent of the legislature that the government of the state take immediate steps to identify any critical thresholds for the health and safety of the people of the state and take all coordinated actions necessary to prevent such thresholds from being reached. An analysis of the above three sections of the law raises the question of what are Òthe critical thresholds for health and safety of the people of the stateÓ? Is it appropriate to simply accept the current standards even if the latest medical studies show them to be outmoded? Is it judicially correct? Is the state to take the attitude that since only a minority of the public will suffer the consequences, a plant such as that described in the SLC DEIS should be allowed to operate? This despite the fact that the Congress of United States has indicated that the term Òpublic healthÓ includes the health of susceptible individuals as well as healthy adults.Ó11Ê

Also, if despite these objections the DEIS is approved, will the permit require daily monitoring of all toxic materials by either SLC or DEC so that an air pollution emergency can be declared in an attempt to stave off the results demonstrated in the current medical literature? If SLC is responsible for daily monitoring, will the results be immediately forwarded to DEC allowing this department to issue an air pollution warning? Apparently, once a permit is issued, it is extremely difficult to amend. Therefore, prudence demands that all necessary health safety requirements are stated explicitly in the permit (should it be issued) if the public is to be minimally protected.Ê

And, finally, considering all of the above, if the DEIS is approved as submitted, would you choose to live one or two miles downwind from this plant? How would you advise a relative with a chronic heart or lung problem who is thinking of making such a move? Would you want someoneÕs asthmatic grandchild to live there? 

Thank you for the opportunity to express my concerns regarding this immense project whose completion will undoubtedly affect the well-being of our community for many decades.Ê

Sincerely yours,Ê



Ira Marks, MD, FAAPÊ


References:Ê

1. Committee on Environmental Health, Amer. Acad. of Pediatrics; Etzel, RA, editor. Handbook of Pediatric Environmental Health, 1999, p.185Ê

2. Samet, J M, et al. Fine Particulate Air Pollution and Mortality in 20 U.S. Cities, 1997-1993. New England J. of Med. 2000; 243:1742-49Ê

3. Peters.A, Liu, E, et al. Air Pollution and Incidence of Cardiac Arrythmia. Epidemiology 2000; 11:11-17 

4. Norris, G. et al. An association between fine particles and asthma emergency department visits for children in Seattle. Environmental Health Perspectives 1999; 107: 489-93Ê

5. Schwartz J. Acute effects of summer pollution on respiratory symptom reporting in children. American Journal of Respiratory and Critical Care Medicine 1994; 150:1234-42Ê

6. Vedal, S et al. Acute effects of ambient inhalable particles in asthmatic and non-asthmatic children. American Journal of Respiratory and Critical Care Medicine 1998;157: 1034-1043Ê

7. Woodruff, TJ et al. The relationship between selected causes of postneonatal infant mortality and particulate air pollution in the United States. Environmental Health Perspectives 1997;105: 608-612Ê

8. Hanley,Q., Koenig,J., Larson,T., Anderson,T., et.al. Response of Young Asthmatic Patients to Inhaled Sulfuric Acid. American Review of Respiratory Diseases 1992; 145:326-331Ê

9. Anderson,K., Avol,E., Linn,W., and Hackney,J. et. al. Controlled Exposures of Volunteers to Respirable Carbon and Sulfuric Acid Aerosols. Journal of the Air and Waste Managaement Association. 1992; 42:770-776Ê

10. Frampton,M., Morrow,P., Utell,M., et.el. Sulfuric Acid Aerosol Followed by Ozone Exposure in Healthy and Asthmatic Subjects. 1995; Environmental Research. 69:1-14Ê

11. S. Rep No. 1196. 91st Cong., 2nd Sess. 9.10 (1970), see also H.R. Rep No. 294, 95th Cong., 1st Sess. 50 (1997)Ê