So what’s next?  How do you get the case restored to the trial calendar?  In our particular case, the matter was venued in Queens.  Pursuant to local TSP part rules, a stipulation is the first option for getting the case restored.  The TSP part can provide a template stipulation which can be signed by all parties to restore the case to the calendar.  The substance of the stipulation states that 1.  all discovery is complete; 2. specifies a date the Note of Issue is to be filed, and 3. specifies a date a conference is to be held, 90 days after the Note of Issue is filed.

In our consolidated action, getting all parties to stipulate to returning the case to the calendar was simply not possible – getting all parties to agree was a non-starter – which leads to the second option for restoring the matter to the trial calendar, a motion to restore.

First, the motion to restore requires an Affirmation of Attempts to comply with the aforementioned TSP part rules.  Simply stated, the Affirmation of Attempts states that you attempted to get all parties to sign the stipulation but were unsuccessful.  In Queens County, the Affirmation of Attempts must be affixed to the Notice of Motion.

Second, the substance of the motion should note that when the note of issue has been vacated, the case reverts to its status as a pre-note case.  Andre v. Bonetto Realty Corp., 32 A.D.3d 973, 974 (2d Dep’t 2006).   Further, in the absence of a 90-day notice pursuant to CPLR 3216, restoring a case marked inactive is automatic.  Matter of Transtechnology Corp. v. Assessor, 71 A.D.3d 1034, 1037-1038 (2d Dep’t 2010); Andre v. Bonetto Realty Corp., 32 A.D.3d 973, 974 (2d Dep’t 2006); Klevanskaya v. Khanimova, 21 A.D.3d 350 (2d Dep’t 2005).

Third, as a practical matter, when the case involves consolidated actions and other parties are hampering or hindering the prosecution of the case, it may be wise to include in the motion to restore a branch seeking severance pursuant to CPLR §603, if required, preferable, convenient, or necessary to restore the matter to the trial calendar.  When arguing in support of severance, demonstrating prejudice to your client is necessary to sever the matters.  Has your client suffered as a result of the delay? Has your client become of recipient of public assistance as a result of the delay?  These two examples can demonstrate prejudice in support of severance.

While restoring a matter to the calendar can be tedious, it is necessary to move the case forward.  Hopefully after reading our blog, restoring a case to the calendar will become a little easier for you – should you end up marked off the active calendar.

Thank you for taking the time to read our blog.

The National Toxicology Program, U.S. Dept of Health and Human Resources, has created a comprehensive report entitled Monograph on Health Effects of Low-Lead, 10/14/2011, peer reviewed November 17-18, 2011. Specifically, this literature makes conclusions on the effects of blood lead levels with a focus on BPb levels less than 10ug/dL.  As described in Section 1.2.2, the NTP’s conclusions were derived by evaluating data from epidemiological studies with a focus on blood Pb levels <10µg/dL.  The evidence is discussed for specific health outcomes within each chapter, and varies by the study design and type of analysis used to examine the relationship of the health outcome with blood Pb across the hundreds of studies evaluated. In some cases, authors restricted the analysis to the population with blood Pb levels <10µg/dL, <5µg/dL, or even lower and the association of the health effect with the blood Pb level is clear.  For example, Lanphear et al. (2000) reported an inverse relationship between blood Pb and academic performance in a cross-sectional study of 4853 children ages 6-16 from the NHANES-III dataset; the association with blood Pb remained significant in further analyses restricted to 4681 children with blood Pb <10µg/dL (p<0.001), and 4043 children with blood Pb <5µg/dL.  In other cases, the authors reported a significant association between blood Pb and an effect in a population with a mean blood Pb level <10µg/dL.   These analyses support an effect of a blood Pb level <10µg/dL, but they do not exclude the possibility that individuals significantly above or below the mean blood Pb level are driving the effect.

As described above, the NTP’s conclusions were derived by evaluating data from epidemiological studies with a focus on blood Pb levels <10µg/dL. The evidence is discussed for specific health outcomes within each chapter, and varies by the study design and type of analysis used to examine the relationship of the health outcome with blood Pb across the hundreds of studies evaluated.  In some cases, authors restricted the analysis to the population with blood Pb levels <10µg/dL, <5µg/dL, or even lower and the association of the health effect with the blood Pb level is clear.  For example, Lanphear et al. (2000) reported an inverse relationship between blood Pb and academic performance in a cross-sectional study of 4853 children ages 6-16 from the NHANES-III dataset; the association with blood Pb remained significant in further analyses restricted to 4681 children with blood Pb <10µg/dL (p<0.001), and 4043 children with blood Pb <5µg/dL.  In other cases, the authors reported a significant association between blood Pb and an effect in a population with a mean blood Pb level <10µg/dL.

Several population based and epidemiologically based peer-reviewed studies and a Federal Report, collectively reach consistent and convergent disease-related outcomes, such studies are then translated into standards of pediatric and medical management of individual children (and adults). Thus, based upon this convergence and consistency in population studies, recently recognized outcomes of childhood lead poisoning have been established. The link between ADHD and lead has been established.

As described above, the NTP’s conclusions were derived by evaluating data from epidemiological studies with a focus on blood Pb levels <10µg/dL. The evidence is discussed for specific health outcomes within each chapter, and varies by the study design and type of analysis used to examine the relationship of the health outcome with blood Pb across the hundreds of studies evaluated.  In some cases, authors restricted the analysis to the population with blood Pb levels <10µg/dL, <5µg/dL, or even lower and the association of the health effect with the blood Pb level is clear.  For example, Lanphear et al. (2000) reported an inverse relationship between blood Pb and academic performance in a cross-sectional study of 4853 children ages 6-16 from the NHANES-III dataset; the association with blood Pb remained significant in further analyses restricted to 4681 children with blood Pb <10µg/dL (p<0.001), and 4043 children with blood Pb <5µg/dL.  In other cases, the authors reported a significant association between blood Pb and an effect in a population with a mean blood Pb level <10µg/dL.  In contradiction to Dr. Molofsky’s opinion, the report specifically states, “In children, there is sufficient evidence that blood Pb levels <5µg/dL are associated with increased diagnosis of attention deficit hyperactivity disorder (ADHD), greater incidence of problem behaviors, and decreased cognitive performance as indicated by lower academic achievement and specific cognitive measures” (Bold added)(The National Toxicology Program of the US Department of Health and Human Services, November, 2011).  The Governmental studies show a direct nexus between elevated lead levels and academic performance in adolescents.

First, a plaintiff is entitled to receive money damages for economic loss and for pain and suffering. Economic loss is awarded to compensate the plaintiff for money that was lost or will be lost as a result of the injury.  For instance, if you were involved in a car accident and were unable to work for a certain period of time you are entitled to be compensated from the liable party for your lost wages.  You are also entitled to be reimbursed for medical expenses along with additional out of pocket expenses that you were forced to pay as a result of the accident.  These numbers can be easily calculated by adding up your lost wages and your lost expenses, a plaintiff is entitled to receive full compensation for all of their past economic damages.

If the plaintiff is continuing to have ongoing medical care and/or is unable to go back to work at the time of the trial/settlement, the injured party may also be entitled to receive compensation for future economic damages.  These damages are more speculative and often necessitate expert witness testimony.  Future economic damages include future medical care, future surgeries and future monetary income from a job that you can no longer perform.  If properly established, a plaintiff is entitled to receive full compensation for these future economic damages.  These medical damages are calculated by adding up your foreseeable medical expenses along with any future medical expenses.  Future lost earnings are calculated by adding up what your future income would have been and may include future raises or promotions that you would have been entitled.

A plaintiff is also entitled to receive money damages for all of the pain and suffering they have endured since the date of the accident, along with the future pain and suffering they continue to endure as a result of the injury.  These non-economic damages are much harder to value and are subjective to the evaluator.  It is interesting to note that the demographics of the County in which you filed your lawsuit have a large impact on how much your pain and suffering is worth.  Statistics show that juries in some New York Counties value pain and suffering greater than other Counties.  Therefore, the same case in one County could be worth substantially more than if it is brought in another County within New York State.  It is a factor that must be considered when initially filing a lawsuit.

Damages can also be reduced depending on the extent of the liability of the defendant party.  If the plaintiff is partially responsible for the accident the value of the case will be reduced by that percentage which is the plaintiff’s own fault.  Also, the plaintiff’s recovery may also be reduced if they have a pre-existing injury which effects the portion of the body which was involved in the accident in question.

While this is by no means a comprehensive description of everything that goes into valuing a personal injury case, it is a basic outline to follow when determining what a case may be worth at settlement or trial.

Municipalities, like any other large bureaucracy, maintain massive amounts of records, files and information.  Specifically relating to the example of our firm’s medical malpractice action, a record containing the costs of home health aide aides are maintained by the New York City Department of Human Resources Administration (http://www.nyc.gov/html/hra/downloads/pdf/services/micsa/hcsp_vendor_rates.pdf).

CPLR §4518(c) provides that “All records, writings and other things referred to in sections 2306 (hospital records; medical records) and 2307 (books, papers, and other things) are admissible in evidence under this rule and are prima facie evidence of the facts contained, provided they bear a certification or authentication by the head of the hospital, laboratory, department or bureau of a municipal corporation or of the state, or by an employee delegated for that purpose or by a qualified physician.

Further, social services agency constitutes a business for the purposes of CPLR §4518.  People v. Montroy, 225 App Div 2d 913 (3d Dept 1996).  Thus, the record of the New York City Human Resources Administration (“HRA”) that contains the costs of home health aid is admissible AND, more importantly, are prima facie evidence of the facts contained, provided the records bear a certification or authentication of the department or bureau head.

Furthermore, the dictates of CPLR §4518(c), provides that “Certain business records may be received in evidence without having been authenticated by their maker, but only if they are certified in accordance with CPLR§4518(c)”.  Peerless Ins. Co. v. Milloul, 140 App Div 2d 346 (2d Dept 1988).

In simpler terms and relating it to our firm’s medical malpractice case, if the record from the HRA is certified or authenticated, it comes into evidence and is sufficient proof of the cost of a home health aid, no costly expert required.

The court in 20-22 Prince LLC v. Tsue Kwai Yen, 32 Misc. 3d 1224(A) (2011) was presented with a situation identical to the situation our firm faced regarding the admissibility of HRA records.  The 20-22 Prince LLC court noted that it was undisputed that the records are certified, and with respect to the admissibility of the records stated that the HRA records can come into evidence under CPLR §4518(c) because they are clearly municipal records that fall within the parameters of the statute.

Equally so, in our firm’s case, the court found that it was undisputed that the records were certified and admitted them into evidence pursuant to CPLR §4518(c) since they were clearly municipal records that fall within the parameters of the statute.  The result, over a half million dollar in additional damages for the cost of a home health aid, and no costly expert needed to prove the damages – now that’s a better way!

Some studies have suggested harmful effects at even lower levels, but the body of information accumulated so far is not adequate for effects below about 10 ug/dL to be evaluated definitively.

At P. 2. The Abstract to the 2007 CDC Report summarizes current knowledge regarding low level lead poisoning:

• “Lead is a common environmental contaminant, and exposure to lead is a preventable risk that exists in all areas of the United States. Lead is associated with negative outcomes in children, including impaired cognitive, motor, behavioral, and physical abilities. In 1991, CDC defined the blood level (BLL) that should prompt public health actions as 10 ug/dL.  Concurrently, CDC also recognized that a BLL of 10 ug/dL did not define a threshold for the harmful effects of lead.  Research conducted since 1991 has strengthened the evidence that children’s physical and mental development can be affected at BLLs<10 ug/dL.”

Indeed, in the years since the 1991 CDC Statement, this have been a spate of studies investigating the effects of low-level lead exposure in children. These papers, published in peer reviewed medical and scientific journals, indicate that blood lead levels below 10 ug/dl cause brain damage in children. See, e.g., [1] Bellijger C., Stiles K.M., Needleman H.L., “Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study.”  Pediatrics, 1992, 90:855-861; [2] Stiles K.M., Bellinger D.C., “Neuropsychological correlates of low-level exposure in school-age children: a prospective study.”  Neurotox Teracol 1993; 15:27-35; [3] Dietrich K.N., Berger O.G., Succop P.A., “Lead exposure and the motor developmental status of urban six-year old children in he Cincinnati prospective study.”  Ped 1993; 91:301-307; [4] Schwartz J., “Low-level lead exposure and children’s IQ; a meta-analysis and search for a threshold.”  Environ Res., 1994;65:42-55; [5] Walkowiak J., Altmann L., Kramer U., Sveinsson K., Turfeld M., Wishoff-Houben M., Winneke G., “Cognitive and sensorimotor functions in 6 year old children in relation to leas and mercury levels: adjustment for intelligence and contrast sensitivity in computerized testing.” Neurotox Teratol 1998; 20: 511-521; [6] Bellinger D.C.., Needleman H.L. “Intellectual impairment and blood lead levels” New England Journal of Medicine, 2003 349: 500; [7] Rogan W.J., Ware J.H., “Exposure to Lead in Children –How Low is Low Enough?, “New England Journal of Medicine 2003 348: 1515-1516; [8] Canfield R.L., Henderson C.R. Jr., Cory-Slechta D.A., Cox C., Jusko TA, Lanphear B.P., “Intelltectual impairment in children with blood leas concentrations below 10 ug per deciliter” New England Journal of Medicine. 2003, 348:1517-26; [9] Canfield R.L., Gendle MH, Cory-Slecta DA, “Impaired neuropsychological functioning in lead-exposed children,” Developmental Neuropsychology 26:513-540 (2004); [10] Lanphear BP, et al., “Low level environmental lead exposure and children’s intellectual function: An International Pooled Analysis,” Environmental Health Perspectives 113:894-899 (2005); [11] Kordas K., Canfield RL, et al. “Deficits in cognitive function and achievement in Mexican first-graders with low blood lead concentrations,” Environmental Research 100:371-376 (2006); [13] Tellez-Rojo MM., Bellinger DC, et al., “Longitudinal Associations Between Blood Lead Concentrations Lower Than 10 ug/dl and Neurobehavioral Development in environmentally exposed Children in Mexico City,” Pediatrics 118:323-330 (2006); [12] Chiodo LM, et al., Blood lead levels and specific attention effects in young children, 29 Neurotoxicology and Teratology 538-546 (Sept.-Oct. 2007); [14] Miranda, ML, et al., “The relationship between early childhood blood lead levels and performance of end-grade tests,” Environmental Health Perspectives 115:1242-124 (2007).

An article in Public Health Reports, by Bruce P. Lanphear, et al., entitled Cognitive Deficits Associated with Blood Lead Concentrations <10 ug/dl in US Children and Adolescents, 13 Pub. Health Reports 521-527 (2000) reports the following results:

• Results.          The geometric mean blood lead concentrations for children in the study sample was 1.9 ug/dl 172 (201%) had blood lead concentrations ≥ 10 ug/dl.  After adjustment for gender, race/ethnicity, poverty, region of the country, parent or caregiver’s educational level, parent or caregiver’s marital status, parent serum ferritin level, and serum continine level, that date sowed an inverse relationship between blood lead concentration and scores on four measures of cognitive functioning.  For every 1 ug/dl increase in blood lead concentrations, this was 0.7-point decrement in mean arithmetic scores, an approximately 1-point decrement in mean reading scores, a 0.1-point decrement in mean scores on a measure of nonverbal reasoning, and a 0.5-point decrement in mean scores on a measure short-term memory.  An inverse relationship between blood leas concentration and arithmetic and reading scores was observed for children with blood lead concentrations lower than 5.0 ug/dl.

Id., at 521. The same study further stated that:

The results of the present analyses suggest that cognitive deficits are associated with blood lead concentrations lower than 5 ug/dl.  Although we did not conduct a formal threshold analysis, these data support the conclusion that thise is, at present, no detectable threshold for the adverse effects of lead exposure on cognitive development or academic disabilities.  These data furthis suggest that more than 12.8 million US children and adolescents born from 1972 to 1988 were adversely affected by environmental lead exposures as indicated by blood lead concentrations >2.5 ug/dl (based on weighting factors and Census data supplied by NHANES [“National Health and Nutrition Examination Survey”]).

In March 2003, the New England Journal of Medicine published an article by Richard L. Canfield, et al., entitled, Intellectual Impairment in Children with Blood Lead Concentrations below 10 up per Deciliter, 348 New England J. Med. 1517 (2003) This scientific study reports adverse effects on IQ of blood lead levels lower than 10 ug/dl:

• Before adjustment for covariates, all four lead measures were inversely and significantly associated with IQ at three and five years of age. The associations did not differ significantly according to age.  From the overall estimate, an increase in the lifetime average blood lead concentration of 1 ug per deciliter was associated with a decrease of 0.87 IQ point: estimates for concurrent blood lead concentrations and average concentrations in infancy were similar; whereas that for the peak lead concentration was somewhat smaller.
• After adjustment for the nine additional covariates, there were significant inverse associations with IQ for all blood lead variables, with no significant differences according to age. The overall estimate indicated that an increase in the lifetime average blood lead concentration of 1 ug per deciliter was associated with a change of – 0.46 IQ point (95 percent confidence interval, – 0.76 to 0.15).  Estimated effects were similar for the concurrent blood lead concentration in infancy and smaller, but still significant, for peak lead concentrations.

The study concludes that:

• Blood lead concentrations even those below 10 ug per deciliter, are inversely associated with children’s IQ scores at three and five years of age, and associated declines are greater at these concentrations that at higher concentrations.

It is established in over 20 peer reviewed articles that the major loss in IQ points occurs at blood lead levels less than 10 ug/dl. These studies converge on a loss of 6 IQ points for blood leads less than 10 ug/dl; and smaller decreases in IQ for blood leads above 10 ug/dl.

The infant brain is undoubtedly sensitive to lead. The rapid of post-natal central nervous system development coincides with a time when infants are engaging in a high degree of hand-to-mouth activity.  Thus, young children living in environments where there are lead hazards can ingest significant amounts of lead dust at a time when their brains are most sensitive to the toxicant’s effects.

Exposure to a lead-contaminated environment can cause injury to an infant even when blood lead levels do not rise above the level defined as lead poisoning by the governmental agencies charged with setting the level that constitutes “poisoning”.

Lead ingestion and resulting injury frequently exists without external manifestations or subjective complaints, that is, without any overt signs or symptoms. For this reason, lead poisoning has sometimes been referred to as a silent epidemic.  Injury in the form of impairment of heme synthesis is an important concept in understating the mechanisms with by ingested lead particles first injure the body.

Injury resulting from lead exposure and ingestion of lead-based paint initially takes the form of an impairment of heme synthesis, that is, the body’s ability to synthesize new red blood cells and heme proteins throughout all the organs in the human body.

When a child begins to crawl and move around in a lead contaminated environment containing lead based paint chips, dust and peeling paint hazards, exposure and ingestion are inexorably contemporaneous.

In such an environment, very small particles of lead-based paint that cannot be seen by the naked eye unavoidably get into the household dust. This dust can come not only from areas of chipping, peeling, cracking paint in an apartment, but also from friction surfaces, such as window sills and doors being opened and shut.  Particles of this size and nature are the general cause of childhood lead poisoning because they totally pervade a child’s living environment and can remain in the environment for months despite normal cleaning routines.

Due to normal hand-to-mouth activities as the infant moves about in a lead-contaminated environment, the ingestion of microscopic lead particles is inevitable and unavoidable. In the case at hand, the infant was observed actually ingesting paint particles.

The primary route of lead absorption is ingestion. Absorbed lead is cleared by the kidneys in the urine and unabsorbed lead is eliminated in the feces.  Absorbed lead is carried throughout the body by the blood within the major burden (+95%) is carried by erythrocytes and the remainder, that most accessible to other tissues, in the plasma.

Lead’s impairment in heme production in a child’s body who is excessively exposed to lead is described in the following excerpt from the 1993 National Academy of Sciences publication:

The aspect of heme-synthesis disturbances by lead that has been most widely exploited as a biologic marker of early effect has been the accumulation of the heme precursor erythrocyte protoporphyrin IX or zinc protoporphyrin (EP or ZPP) in blood of children and in some adult populations.  EP accumulates in response to lead-related inhibition of the activity of the intramitochondrial enzyme ferrochelatase or lead-related impairment of intramitochondrial iron transport [Citations omitted] EP increase therefore indicates a generalized mitochondrial toxic response.

Heme synthesis impairment is a bodily injury by any definition and impairment of heme synthesis can be present without elevation in blood levels.