|Fraser v 301-52 Townhouse Corp.
|2006 NY Slip Op 51855(U) [13 Misc 3d 1217(A)]
|Decided on September 27, 2006
|Supreme Court, New York County
|Published by New York State Law Reporting Bureau pursuant to Judiciary Law § 431.
|As corrected in part through October 16, 2006; it will not be published in the printed Official Reports.
COLIN FRASER, PAMELA FRASER and ALEXANDRA FRASER, an infant by her parents and natural guardians, COLIN FRASER and PAMELA FRASER, Plaintiffs,
301-52 TOWNHOUSE CORP. and JANICE JOHNSON, Defendants.
This action was brought to recover, inter alia, for personal injuries allegedly arising from plaintiffs' water-damaged apartment. All allegations of personal injury except for respiratory problems, rash and fatigue, were withdrawn.[FN1] Defendant moved for a Frye hearing to determine whether the plaintiffs' theory of the case — "that mold in their apartment caused them respiratory problems - is generally accepted in the relevant scientific community and whether the methodology used by plaintiffs to measure the mold, was within generally accepted scientific methods." Court's June 21, 2005 decision. The hearing later was expanded to address causation of respiratory problems by water-damaged buildings.
A ten-day Frye hearing followed, encompassing more than one-thousand pages of testimony and the introduction of more than seventy scientific articles and books.
I. Findings of Fact
A. Mold Sampling Report
The March 31, 2002 Olmstead Environmental Survey of plaintiffs' apartment was introduced into evidence as plaintiffs' 6, to demonstrate its methodology and results. The report describes the six-story, brick building in which the apartment is located as a concrete and steel structure with plaster walls, located on the North side of 52nd Street, East of Third Avenue. The [*2]apartment consists of the first floor and basement level of the building. Air, bulk [FN2] and wipe [FN3] samples were collected on March 13, 2001. One air sample was taken from the backyard garden, and two air samples were taken in the basement office, near the glass windows. The report noted that "there are no regulatory or reference levels of mold growth" and "no regulatory standards or recommended standards for numerical levels of bioaerosols in air."
The Olmstead testers found that the outdoor air sample was dominated by Basyidiomycetes mold with a total mold level of 171 colony forming units per gram of material ("CFU/g"). The two indoor air samples were dominated by Aspergillus versicolor mold with 495 CFU/g and 836 CFU/g, amounts the report described as "clean."
Two bulk samples were taken, one from the wall along the glass door and one from the wood floor at the North windows. The bulk sample from the wall showed no detectible mold growth. The bulk sample from the floor showed 209,000 CFU/g. Wipe samples were taken from the Northeast corner wall by the glass doors and from the wood floor near the glass doors. The wipe sample from the wall had 14,000 CFU/g dominated by Aspirgillus versicolor, and the floor sample merely had elevated mold growth, without any CFU/g count, dominated by Rhodotorula glutanis.[FN4] No measurements were taken for moisture, endotoxins, mycotoxins, [*3]Beta-D-glucans or Volatile Organic Compounds (VOCs) or Microbial Volatile Organic Compounds (MVOCs).
B. Dr. Eckardt Johanning's March 28, 2005 Medical Reports
The March 2005 medical reports for the three FRASER plaintiffs were introduced as Defendant's Exhibits A1-A3.
Colin Fraser, who was 44 years old, worked from home, was not exposed to dangerous chemicals and had four cats during all relevant periods. He denied a history of allergy, asthma or eczema. In August 1996, he and his family moved into the subject apartment at 301 East 52nd St., New York City, and he developed a leg rash, lethargy, focusing and hearing problems, congestion, nasal mucus production and throat itchiness. His symptoms improved when he left the apartment. In December 2002, he and his family moved to Woodstock, New York, and he is feeling better. Sporadically, he still has leg rashes, and he continues to complain of memory, focus and stamina problems. When in damp, dusty areas, he gets a sore throat, sneezes, has eye irritation, itchiness and mucus production.
In July 2003, immunological and allergy testing for him, were normal. "Selected IgE testing to Aspergillus fumigatus, Cladosporium herbarum and Penicillium notatum was normal." Immunoglobulin IgG showed a reaction to Micropolyspora faeni, Thermoactinomyces, Alternaria, Aureobasidium pullulans, Phoma herbarum and Trichoderma viride. In February 2005, the immunoglobulin testing showed an elevation of these fungi and a reaction to Aspergillus alternata, Aspergillus fumigatus and Penicillium notatum. When evaluated by a pulmonologist, Mr. Fraser's pulmonary function studies showed a restrictive lung pattern. Dr. Johanning concluded "that Mr. Fraser had a history of acute irritant allergic-type reaction while he was living and working at his previous apartment at 301 East 52nd Street."
Pamela Fraser, has worked with her husband since 1997. She moved into the cooperative apartment with her husband and reported developing problems related to her nose, teary eyes, itchiness, productive cough, shortness of breath, sore throat, wheezing, physical and mental fatigue, forgetfulness and depression. Neuropsychological evaluation found significant cognitive impairment. Mrs. Fraser stated that she feels better since moving to Woodstock, but still has respiratory problems and suffers from fatigue and memory loss. Other than allergies to penicillin and sulfa drugs, Mrs. Fraser had had no allergies or asthma, but has been diagnosed with lupus, hypothyroid, anemia and depression.
When tested in 2003, Mrs. Fraser showed a reaction to house dust, but was otherwise normal except for lower than normal IgG. IgG showed a reaction to Micropolyspora faeni, Thermnoactinomyces and Trichoderma viride. In 2005, the IgG antibody showed a mild reaction to Micropolyspora faeni and Thermnoactinomyces. When seen by a pulmonologist in 2005, the pulmonologist found rhino sinusitis and environmental airway disease. Dr. Johanning concluded that Mrs. Fraser had allergic and irritant-type reaction as a result of living in the cooperative apartment.
Alexandra Fraser, was born in 2001 and moved from the cooperative apartment in December 2002. Her parents recounted that Alexandra developed health problems [*4]while living in the apartment. She was diagnosed with an upper respiratory infection. She has been doing better since moving to Woodstock, but had pneumonia in 2004 and frequently suffers from colds. Dr. Johanning found a history of respiratory problems.
C. Scientific Writings
According to the witnesses, the following scientific writings, articles and books are peer-reviewed and published in journals generally accepted in the medical and/or scientific community. They demonstrate that, with the exception of one article, the scientific research has not established that indoor exposure to mold causes the symptoms for which the plaintiffs seek to recover in this action. Although some of the literature found that indoor mold exposure or dampness had an "association" with transient upper respiratory problems in adults (symptoms similar to those of the common cold), or a "strong association with asthma in children, these findings fall short of a finding of "causation." Moreover, it is generally accepted in the scientific community that standard, reliable methods of measuring indoor airborne mold do not exist and that multiple airborne sampling on different days must be done to get an accurate reading. A summary of the articles admitted into evidence follows:
Plaintiffs' 1, Respiratory Morbidity in Office Workers in a Water-Damaged Building, published in January 2005, reported that occupancy in a water-damaged building "can be associated" with the onset and exacerbation of respiratory health conditions. The study used allergen skin prick testing using dust mite mix, cockroach mix, cat hair, grass mix, ragweed mix, common weed mix, tree mix, outdoor mold mix, aspirgillus mold mix and Penicillium mold mix. Atopy, the genetic tendency to develop classic allergy diseases, was defined as at least one positive skin test of the seven common antigen extracts, excluding the mold extracts. The study found an increase in asthma incidence in the period after building occupancy. Moreover, it noted: higher nasal and eye symptoms than lower respiratory symptoms, but less than those of U.S. adults; lower rates of wheezing and lifetime and current asthma than in the adult U.S. population; and improvement in "reported" wheeze, nasal and eye symptoms when away from work. Finally, the study noted that it was limited by the "possible influence of participation bias."
Plaintiffs' 2, Children's Health: Home Dampness and Molds, Parental Atopy, and Asthma in Childhood: A Six-Year Population-Based Cohort Study, published in March 2005, reported on a six-year, population-based prospective cohort study of 1,916 children up to the age of seven, which focused on asthma. The study looked at parents with asthma or allergic rhinitis and homes with a history of water damage, which had moisture problems, visible mold and mold odor. The study found that: children with parental asthma increased the incidence rate of asthma by more than 100%; the effects of maternal or paternal rhinitis increased the incidence rate by 71% and 54% respectively; children living in homes with mold odor had more than an 100% increase incidence rate of developing asthma; but a history of water damage, moisture in the interior surfaces and visible mold did not predict asthma. Here too, confounders such as self-reporting, information bias and other indoor environmental factors were present.
The Fraser case does not involve a child with asthma.
Plaintiffs' 4, Clinical Experience and Results of a Sentinel Health Investigation Related to Indoor Fungal Exposure, published in June 1999, recounted a study based on self-reported exposure to indoor fungus. It found that "[children with preexisting, significant immunological [*5]weaknesses and defects are at increased risk and should be protected from unnecessary fungal exposure." The Fraser case does not involve immuno-compromised children.
Plaintiffs' 7, A Review: Fungal Exposure Assessment in Indoor Environments, published in January 2001, addressed the methodology in determining fungal exposure in buildings. The article began by noting that "clear dose-response relations in damp buildings are missing because of difficulties in the fungal exposure assessment and lack of standardized protocols for fungal sampling and analysis." The article continued by stating that "no single method may be appropriate for the extensive identification of fungal growth and fungal exposure assessment[,]" and that there is a difference both in the type of fungus and the percentage of culturable spores shown between dust and air samples from the same interior space. Additionally, the article pointed out that the capability of spores to become airborne varies by type of fungal spore, that the shorter the sampling time, the less representative the sampling of the air, and that problems identifying fungal composition, especially Penicillia, Aspergilli and Fusaria, always exist. Most important, the article noted that Beta-D-glucan "has been considered to be most appropriate" for measuring fungal biomass because exposure to it
may have a role in inflammatory responses in humans. Considerably
less evident causative agents are MVOCs which were originally and are
still used in the detection of moisture problems, hidden biocontamination
and odor complaints in buildings....some studies have shown that those compounds alone are hardly responsible for sensory irritation symptoms
at the concentrations reported in damp buildings...no analytical method
for the determination of airborne toxins in indoor environments is available
at the present time.
Finally, emphasizing the need for more information regarding the effects of indoor fungal exposure on health, the author stated that no analytical method for determining airborne toxins in indoor environments is presently available. The author did note that Dr. Johanning uses biomonitoring and measures IgG, IgE and IgA antibodies to assess fungal exposure and allergic response in indoor air, but he criticized this method as problematic. He ended by positing that "fungal exposure at indoor-air allergen concentrations does not induce allergic reactions of known types."
Plaintiffs' 8, Bioaerosols, Fungi, Bacteria, Mycotoxins and Human Health (3/2005), a book edited by Dr. Johanning, contains a number of articles bearing on the subject of this hearing. The court will consider only the articles it deems relevant and those that it, as a lay person, understands:[FN5]
I) An article written by Torben Sigsgaard of Denmark and Carl-Gustaf Bornehag of Sweden, is a review of the literature on damp buildings and associated health effects. The article states that "there is strong evidence [that] moisture related problems in buildings increase the risk of health effects" among children and adults and that "the most important health effects that are associated to dampness in buildings seem to be airway symptoms such as wheezing, cough and asthma." The article, however, warns that the literature is not conclusive as to the causative [*6]agents for these health effects and that the suggested agents are mites, microbiological agents and organic chemicals from degraded building material. The article states that there is a strong need for more studies.
ii) Mold Remediation of a School and Teachers' Health, by a group from Finland, studied teachers at one school before and after mold remediation. The small group of teachers self-reported their symptoms. The article found a higher incidence of sinusitus and sick leave in the group. The group produced eight reported asthma cases. After remediation, reports of symptoms of allergic rhinitis, bronchitis and conjunctivitis decreased and no new asthma cases appeared.iii) Mold Toxicity: Risk Assessment For Humans Exposed Indoors by Harriet M. Ammann, emphasizes how little is known about risks from toxic exposures to molds and mold products in the indoor environment. The article states that determining exposure is "highly imperfect" due to the dearth of animal studies, the problems with reconstructing past exposures, the confounding factors of other allergic agents and contaminants, the difficulty in diagnosis since the symptoms are not unique and the imperfection of methods to measure toxins.
iv) Tuula Putus in Health Effects Of Moisture Damage Associated Microbes, published by The National Public Health Institute, reviews the current knowledge on health effects of indoor air microbes and makes the following observations - damp building complaints encompass unpleasant odors, emission of chemicals from the construction materials, organic and inorganic dust and mites; temperature, humidity, draft and odors affect chemical and microbiological contamination; airborne mold concentrations and health effects do not correlate well and, therefore, surface and material samples are preferred; mold exposure and respiratory symptoms and infections are associated; the underlying mechanism between this association is unknown; mold allergy is more common in children than adults; and more research is needed.
v) Systemic Improvement After Cessation of Mold Exposure: Clinical Experience in Environmental and Occupational Health, by Iris Udasin, Howard Lu, Robert Laumbach and Howard Kipen , notes that "the most generally accepted pathophysiological explanation for mold-related symptoms" is allergy. Ten percent of Americans have allergic reactions to fungal antigens, but only 5% have clinical symptoms. The article states:
Fungal infections are not thought to comprise a significant risk
in healthy people. To date, studies have not clearly demonstrated
a causal relationship between mold exposure and non-allergic
vi) Do MVOCs Cause Irritation: Nasal Effects of VOCs and VOC Oxidation Products in Controlled Human Exposures, by a group of researchers from UMDNJ and Rutgers, states that concentrations of MVOCs in indoor air are low compared to levels known to cause acute irritation in animals and humans. The study exposed 135 healthy women to three minute exposures and found that "MVOCs appear to be unlikely to cause acute upper respiratory irritation in mold-contaminated buildings." The report notes that the air concentration of MVOCs in mold-contaminated buildings is much lower than the exposures in the study.
vii) Aino Nevalainen in Exposure in Moldy Buildings, begins by noting that "the association between moisture and microbial growth and adverse health effects among the [*7]occupants has been shown in a number of epidemiological studies (Bornehag et al. 2001), but the causal connections between various exposing agents and the health endpoints are not well known." She writes that "no conclusive evidence [exists] that increased concentrations of fungi in indoor air would be the actual cause for [respiratory] symptoms." She further notes that viable fungi in indoor air represent only 1% of airborne particles in indoor air, but that the health effects of exposure to endotoxins, glucans, bacteria, VOCs, and microbial toxins, which are also in the air, have not been shown. She concludes by stating that "exposure in moldy indoor environments is a complex issue, and little causal connections to health effects have been shown so far."
viii) Sampling: A Neglected Part of Building Investigations and Microbial Exposure Assessment, by Anna-Lisa Pasanen, notes that the most important properties for air sampling are representativeness, reliability and ease of use. The article states that different sampling methods serve different purposes and suggests that bulk and surface samples are useful for detection of microbes and air sampling can be used to find out whether microbes are spreading from the contaminated areas.
ix) A group of scientists from the University of Cincinnati in Release of Aspergillus Versicolor Fragments and Spores From Contaminated Surfaces, observe that although epidemiological studies have shown that individuals in buildings with mold, have more respiratory symptoms and diseases, no clear cause-and-effect relationship has been well-established between health effects and airborne fungal spores. They note that field studies have shown that airborne fungal spores in mold problem buildings are the same as in non-problem buildings. The authors, therefore, posit that fungal fragments may be the potential source of the health effects.
Plaintiffs' 9, Bioaerosols, Fungi and Mycotoxins: Health Effects, Assessment, Prevention and Control (5/2001), a book edited by Dr. Johanning, contains a number of articles bearing on the subject of this hearing. Several articles in this book were introduced by plaintiff. They are:
I) Effects After Mold Exposure Which are the Causative Agents?, by Roger Rylander, which notes that although field studies can describe relationships between agents in molds and the effects caused by exposure to mold, the specific proof needed to find causality is difficult to achieve. Nonetheless, the paper reviews structural and metabolic agents and contends that the general medical effects of mold exposure are airway inflammation, allergic reactions, weakened resistance to infection, neurological effects and cancer.
ii) Ecology, Detection and Identification Problems of Moulds in Indoor Environments, by Robert A. Samson, lists many mycotoxins found in indoor environments that are produced by mold species and concludes that the presence of indoor mold should be detected through "direct visual inspection" and lab tests, rather than by attempting to gage the quantity of airborne propagules/spores.
iii) Indoor Moulds: A Public Health Problem in Belgium: Overview of 15 Years' Experience, by Nicole Nolard, is a survey of 400 individuals, who reported respiratory disorders of allergy and asthma, over a 15 year period. One hundred and thirty homes were found to have fungi. Asymptomatic individuals were found to live in the same homes as those with allergic reactions and asthma.
iv) Pilot Analysis of the Immune Response to Fungal Antigens in Subjects Working in [*8]Humidity Damaged Houses, by a group of scientists from the University of Oulu in Finland, discusses the presence or development of specific antibodies in people living in humidity-damaged houses. It suggests that antibodies do not prove that these people's health problems are a result of exposure to molds. According to these authors,
"studies have not been published to document the effect of mold antigens on lymphocyte function in cell cultures."
v) Can Microbial Volatile Metabolites Cause Irritation at Indoor Air Concentrations?, by a group of scientists from the University of Kuopoi in Finland, evaluates the risk related to exposure to MVOCs in buildings with moisture problems. The paper suggests that "microbial growth in construction should not increase the probability of irritating symptoms considerably." It further states that microbial growth in construction has a minimal effect on the overall VOCs possibly related to microbial growth in moist, moldy buildings and is usually low enough that they should not cause sensory irritation in humans.
vi) Clinical Findings Related to Indoor Fungal Exposure Review of Clinic Data of a Specialty Clinic, by Eckhardt Johanning & Paul Landsberg, reviewed 151 self-reported cases of patients at a "specialty clinic." There was no control group. The patients filled out questionnaires reporting work-related and residence-related exposure to water damaged buildings caused by a "variety of natural or man-made causes including flooding, severe weather (storms), snow and ice damage, roof leaks, building envelope defects, wall condensation, sewage backup, earthquake and water damage by firefighting." The study could find no "clear trend of clinically detectable immune suppression or modulation" and acknowledged that it had methodological limitations and could "not claim to prove causation for specific diseases."
vii) Symptoms Associated to Work in a Water Damaged School Building, by a group of scientists from Aarhus University in Denmark, studied a water-damaged school infested with mold as related to the health of 45 employees. It found employees complaining of headache, tiredness, nausea, sleep difficulties and episodes of fever, shivering or flu-like symptoms. The paper notes the need for a standardized way to investigate water-damaged buildings and states that there is a dose response relationship between exposure to water-damaged buildings and symptoms of inflamation and irritation.
viii) Building-Related Illness in Occupants of Mold-Contaminated Houses: A Case Series, by James Craner, dealt with "sick building syndrome," studying only five cases in Nevada and Utah. "Sick building syndrome" was defined as causing inflamed mucous membranes, respiratory tract and skin problems, fatigue and neurocognitive dysfunction. The study found that removal from the contaminated indoor environment led to a relatively rapid health improvement in most of the cases. The paper recognized that "large gaps in clinical, pathological, epidemiological and exposure assessment remain in determining the causal relationship between indoor fungal contamination and [sick building syndrome]."
ix) Fungal Exposure and IgG-Levels of Occupants in Houses With and Without Mold Problems, by a group of scientists from Kuopio, Finland, evaluated the relevance of serum antifungal-IgG antibodies to reflect exposure to building related fungi. The study found that high IgG levels are likely caused from exposures other than from the studied damp homes and that IgG levels do not show where and when microbial exposures take place.
x) Moisture Observation and Health, by a group of Finnish scientists, studied two [*9]tenements with moisture problems and health effects of people living in these buildings. Observations of dampness and moisture in the buildings were used "as a proxy" for indoor microbial growth. The paper concludes that "[no serious health effects were associated with exposure to moisture." However, it states that respiratory symptoms and infections were higher in the studied buildings.
xi) Anatomy of a Fungal Problem, by Neil Carlson and Arif Quraishi, addresses methods of sampling mold in a school with visible fungal growth. The paper suggests that viable fungal sampling should be the only method for conducting risk assessment relating to exposure to fungal spores and bioeffluents.
xii) Fungal Growth in Buildings: The Aerobiological Perspective, by Harriet A. Burge, speaks to the difficulty of assessing health risks associated with fungal growth in indoor environments. The paper states that hypotheses development and testing processes that result in cause/effect relationships are necessary "to accurately determine the role of indoor fungi in human disease." Consequently, the paper notes that aerobiologists conclude that a useful method to understand disease contracted through inhalation of airborne agents, is to trace the agents' pathways. The paper describes S. Chartarum and its tendency to grow in indoor building materials under wet and cool conditions. As described by the paper, response to large doses of S. Chartarum in laboratory animals and in-vitro studies, is the product of potent cytotoxins leading to the release of inflammatory mediators, cell death and hemorrhage. Further, ingestion by people of this fungus produces symptoms. However, the paper notes that "inhalation exposures cannot be unequivocally said to result in adverse health effects." The paper concludes by stating: "There is reasonable evidence that aerosol release from S. Chartarum colonies is minimal, and that, except under very active disturbance, aerosol levels are unlikely to reach concentrations that would lead to significant pulmonary deposition in adults or children." The paper suggests that much research needs to be done before one can assert that S. Chartarum is a likely cause of building related illness.
xiii) Why Are There Still Problems With Fungal Allergen Extracts?, by W. Elliott Horner and Samuel B. Lehrer, addresses the difficulty and unreliability of work with allergen extracts of fungi.
xiv) From Fungal Exposure to Disease: A Biological Monitoring Conundrum, by Raymond E. Biagini, addresses biological monitoring and the estimation of exposure to an agent through the measurement of biomarkers resulting from an internal dose of the agent. The paper states:
Numerous investigators have implicated putative exposure to macrocylic tricotheces and other compounds from Stachybotrys chartarum as being associated with a plethora of signs and symptoms of disease. To date, no compelling biological marker evidence for exposure to Stachybotrys chartarum mycotoxins or their metabolites has been presented. There is no doubt that exposure to Stachybotrys chartarum is associated with an increased prevalence
of self-reported symptoms. However, evidence of the association of these complaints with frank disease is lacking.
Plaintiffs' 10, The Court will not consider this exhibit, since these book chapters were not [*10]peer-reviewed and they contain anecdotal evidence and hypotheses.
Plaintiffs' 11, Adverse Health Effects Among Adults Exposed to Home Dampness and Molds (1990), a Canadian study, found that home dampness and mold "may be" a risk factor for respiratory disease in the Canadian population. The study involved self-reporting individuals. Fungal spores were not measured, and dampness was assessed by the participants' "perception of home dampness." The study recommended future research.
Plaintiffs' 12, Effects of damp and mould in the home on respiratory health: a review of the literature (1998), by Dr. Jennifer Peat and J. Li of Sydney University Department of Pediatrics, and J. Dickerson from the Institute of Respiratory Medicine at the University of Sydney, is a review of 15 years of studies on the health consequences of dampness since "it is thought to have health consequences because it has the potential to increase the proliferation of house-dust mites and moulds, both of which are allergenic." The review notes that it is difficult to compare studies because the methods of measuring exposures differs in each, but finds the most reliable studies dealt with children. The paper further notes that Alternaria from outdoor sources has been associated with asthma exacerbation, but that Cladosporium, Penicillium and Aspergillus do "not appear to have clinical importance in terms of being a risk factor for the development of asthma" and that these molds are "less potent than Alternaria in causing airway abnormalities." The review observes that "the two symptoms most often investigated are cough and wheeze and [t]he increased risk of having these symptoms if the home is damp or mouldy is fairly small."
Plaintiffs' 15, Bioaerosols, Assessment and Control, a textbook published by the American Conference of Governmental Industrial Hygienists, is a compilation of articles about bioaerosols (airborne particles that are living or originate from living organisms) and biologically derived airborne contaminants (bioaerosols, gases and vapors produced by living organisms). The introduction cautions that, in the United States, there are no threshold limit values (air concentrations standards that represent conditions which would have adverse health affects on those repeatedly exposed) for bioaerosols in non-work environments due to insufficient data and information. The book "defines methods for assessing and controlling exposures to biologically derived airborne contaminants."
Plaintiffs' 16, Field Guide for the Determination of Biological Contaminants in Environmental Samples, a guide published by The American Industrial Hygiene Association, is a compilation of articles speaking of air sampling. The introduction notes that "there is a lack of universally accepted exposure limits or guidelines."
Plaintiffs' 17A, Occupational and Environmental Lung Diseases: Overview for Family Physicians, is a book chapter written by Eckardt Johanning. The chapter begins by admonishing that the "family physician should consider the possibility of occupational exposure [to inhalation of organic and nonorganic materials] in every adult patient with problems of the upper or lower airway." Dr. Johanning states that acute and chronic lung disease is "associated" with inhalation of organic and nonorganic materials found in the workplace and that workplace exposure to chemicals, gases, particulates and dust can cause rhinitis, laryngitis, bronchitis, asthma and chronic
obstructive lung disease. He lists occupations and industries with high risk and admonishes the family practitioner to consult with a lung specialist or occupational health consultant for accurate [*11]diagnosis and treatment. The chapter focuses on work- related exposure and disease.
Plaintiff's 17B, Indoor Environmental Quality, is another book chapter written by Eckardt Johanning, this one concentrating on "scientific evidence of sick building syndrome.'" He cites the statistic that one-third of United States buildings have serious indoor air quality problems. He, however, does acknowledge that only a small percentage of the millions of workers who complain about indoor air quality develop serious illness, that the complaints may well be related to work problems and that determining the single cause of illness is difficult.
Dr. Johanning notes that there is an "association" between health problems and exposure to moisture and microbes in buildings. Wet building materials can cause growth of fungi and bacteria and can contaminate indoor air. He continues by stating that serious toxic or allergic reactions are linked to large amounts of indoor Stachybotrys atra, Aspergillus fumigatus, A. Versicolor, Paecilomyces variotti, Penicillium and Fusarium.
Plaintiffs' 18, focuses on work-related diseases and injuries.
Plaintiffs' 19A-I , consists of articles published in The Journal Of Allergy and Clinical Immunology:
19A, is the introductory article. It contends that there are studies linking sleep disorders with health problems and that allergic rhinitis may be a cause of sleep disorder.
19B, states that allergic rhinitis can impair sleep, leading to daytime fatigue. The article further states that the efficacy of certain medications in improving such sleep disorders has been established, through multiple randomized, double-blind clinical trials.
19C, this article focuses on allergic rhinitis in children.
19E, contends that nasal congestion, a common symptom of allergic rhinitis, is often associated with poor sleep quality, which leads to decreased learning ability and work productivity.
19F, this article notes that allergic rhinitis is the most common atopic disease in the United States and is estimated to affect 25% of adults and 40% of children. The article speaks to the pathology of this disease, which is similar to the pathology of asthma, and discusses the treatment.
19G, reports on a study seeking to investigate the effects of seasonal allergic rhinitis on sleep and quality of life. The study found significant disparities in results with impaired daytime sleepiness and poorer quality of life related to the severity of the disease.
19H, this article repeats the facts that: the symptoms and pathology of allergic rhinitis can interfere with sleep quality, that 24% of adults and 40% of children in the United States suffer from allergic rhinitis and that sleep disturbance affects daytime energy, mood and function.
19I, addresses the symptoms of allergic rhinitis and their effect on quality of life.
21A, is a 1988 Canadian study investigating the association between home dampness, mold and health, which was conducted through questionnaires. The study found that home dampness and mold were "associated with increased [respiratory] symptoms in adults." The study did not measure fungal spores.
21B, is a 2002 paper, written by a Dr. John Santilli (the article does not set forth his credentials) of Bridgeport, Connecticut, which studied mold exposure in two public schools. It [*12]begins by stating that clinicians and the general public have become increasingly aware that "mold is a significant cause of allergic diseases." It notes that there are no standardized methods for testing indoor air quality, no methods for assessing health impacts from exposure to mold in schools and "no quantitative standards for determining what level of mold contamination is hazardous." It continues by stating that fungi can cause inflammatory reactions, especially in immuno-compromised individuals and contribute to asthma, allergic rhinitis and dermatitis in sensitized individuals. It then states that mold produces mycotoxins which can cause, among other things, mucous membrane irritation, skin rash, nausea, immune system suppression, liver damage, central nervous system damage, Scleroderma, endocrine effects and cancer. However, the article cautions that more study and research is necessary to determine the health impact of mold inhalation. This paper is replete with generalities, evaluated only twelve teachers in one school and four individuals in the other school and is not specific when discussing types of mold. Due to these factors and the lack of credentials for the author, the court will not give it great weight.
21C, is a 2002 German study of children which concluded, "elevated indoor concentrations of molds in wintertime might play a role in increasing the risk of developing atopic symptoms and allergic sensitization not only to molds but also to other common, inhaled allergens." The findings were "limited by methodologic difficulties of quantifying molds and by the relatively small number of homes studied."
21D, in this 2000 Finnish article, the relation between damp homes and respiratory symptoms was studied with self reporting questionnaires. The strongest association was found between visible mold and asthma and common colds. The study concluded: "The risk of current asthma, allergic rhinitis, and atopic dermatitis was higher in damp homes. Of the respiratory infections, the risk of common colds was most clearly increased."
21E, a 1994 Dutch article, studied symptoms and respiratory infections in occupants of mold problem houses and day care centers. The study found that exposure to molds caused by moisture problems was associated with a higher prevalence of respiratory symptoms and recurrent respiratory infections requiring antibiotic treatment.
21F, was a portion of a March 2001 U.S. Environmental Protection Agency booklet entitled Mold Remediation in Schools and Commercial Buildings. A portion of an appendix to this booklet was introduced, which made general statements regarding the potential effects of "mold", without attribution and specificity. The court will not give this exhibit great weight.
21G, is a 1998 Swedish article about a workshop studying children's health and indoor mold exposure. The article states that exposure to mold and/or dampness in homes may constitute a health risk to children resulting in respiratory symptoms, an increased risk of infection and skin symptoms. The article notes that children's immune systems are not fully developed. It suggests testing with skin prick and IgE markers. The pathological mechanism for the respiratory symptoms is identified as inflammation. The study speaks to the difficulty of measuring mold growth.
21H, is a 1994 Finnish study regarding workers in water-damaged day care centers. It found that work-related eye and respiratory symptoms were higher among the day care workers exposed to both water damage and mold odor.
21J, is a Swedish paper published in 2000, which explores the structure and immune [*13]system influence of (1-3)Beta-D-glucan, a type of polymer found in microorganisms and plants. This polymer was not measured in the Fraser apartment, and the court, therefore, will not consider this article.
21K, is a 1999 article which speaks to clinically assessing mold exposure and testing for it. It notes that allergy skin test material is unavailable for most airborne fungi and those that are available are not standardized. The article emphasizes the importance of air sampling data but notes that such sampling is dependent on the method of analysis.
21L, is an article which focuses on infants in the first year of life and is not relevant to this case.
21M, is a 1992 Dutch article reporting on a study of damp houses and adult respiratory symptoms. The self-reporting study found a strong association between cough and phlegm and living in a damp home. It found a weaker association between dampness and wheeze and asthma, and it found little association between living in a damp home and allergy to house dust.
Plaintiffs' 23, is a book entitled Damp Indoor Spaces And Health, published in 2003 by the Institute of Medicine of the National Academies. The book is a scientific review conducted in accordance with the rules of the National Research Council's Report Review Committee. The report was compiled by a committee of experts at the request of the Center for Disease Control. Its mission was to review the scientific literature regarding the relationship between damp or moldy indoor environments and the manifestation of adverse health effects, particularly respiratory and allergic issues. The committee looked at studies and articles through 2002, evaluating them for relevance, scientific methodology, validity, bias and confounding factors.
The report came to the conclusion that evidence in 2003, was not sufficient to conclude that a causal relationship exists between health outcomes and damp/moldy indoor environments. Sufficient evidence, as used in this statement, was defined as meaning "that the exposure can cause the outcome, at least in some people under some circumstance." The report concluded that "[t]here is sufficient evidence of an association between exposure to a damp indoor environment and upper respiratory tract symptoms" and "sufficient evidence of an association between presence of mold' in a damp environment and upper respiratory tract symptoms." This means that the evidence is sufficient to conclude that there is an association between the agent and outcome observed in studies in which chance, bias, and confounding can be ruled out with reasonable confidence. In regard to the upper respiratory tract (nose, mouth, sinuses and throat), the committee identified the following symptoms studied: rhinitis, an inflammatory condition involving the nasal mucosa and causing nasal congestion, sneezing and runny or itchy nose; sinusitis, similar to the common cold; ear and eye symptoms. The report further found sufficient evidence of an association between exposure to a damp environment/mold and cough and wheeze and asthma symptoms in sensitized asthmatic people.
The committee further found that there is limited or suggestive evidence (this means chance, bias and confounding in the study could not be ruled out) of an association between exposure to a damp indoor environment/mold and episodes of shortness of breath, the development of asthma or lower respiratory illness in otherwise healthy children. The committee found inadequate or insufficient evidence (this means insufficient quality, consistency or statistical power in the study or no study) to determine whether an association exists between the presence of mold or other agents in damp indoor environments and episodes of shortness of [*14]breath, the development of asthma or respiratory illness in adults. The committee found inadequate or insufficient evidence to determine whether an association exists between either exposure to a damp indoor environment or mold and/or other agents found in damp indoor environments and: the presence of airflow obstruction in otherwise healthy people; mucous membrane irritation syndrome; chronic obstructive pulmonary disease; and skin symptoms. Finally, the committee found no studies associating fungal sinusitis with damp or moldy indoor space and noted that fungal colonization is often found in the sinuses of healthy persons. [FN6]
The report also made the following observations:
The definition of "dampness", as used in the various studies reviewed, is
very vague. Excessive indoor dampness is not by itself a cause of ill health. However, it attracts dust mites, cockroaches, rodent infestation and the initiation of chemical emissions from building materials.
There is no generally accepted definition for "dampness", and there is no single cause of excessive indoor dampness.
All indoor space contains microorganisms, fungi and bacteria. Common indoor fungi are Cladosporium, Aspergillus, Penicillium, Alternaria and Saccharomyces. The types of mold vary by geographic area, climate, season, weather conditions and individual sources.
There is a lack of knowledge of the role microorganisms play in exacerbating disease, due in large part to the lack of valid quantitative exposure-assessment methods and knowledge of which species of mold affects health. Microbial exposure assessment is subject to large measurement errors and biased exposure/response relationships. The process of fungal-spore aerosolization is poorly understood. Moreover, methods for assessing human exposure to fungal agents is poorly developed. Counting cultured colonies and spores have an uncertain relationship to allergen, toxin and irritant content of exposures. Interpretation of indoor sampling should be based on multiple samples.
Most of the information regarding the toxic effects of fungi and bacteria is derived from in vitro and animal studies. In vitro studies are not suitable for human risk assessment. Risk assessment, however, can be extrapolated from animal studies but only if chronic exposure has produced sufficient information, taking into account species differences and dose exposure. Animal studies are useful for generating hypotheses.
In vitro and in vivo studies establish that exposure to microbial toxins can
occur via inhalation and dermal exposure and through ingestion. The dose required to [*15]cause adverse health effects in humans has not been determined. Immunotoxic, neurologic, respiratory and dermal responses may be caused after exposure to specific toxins, bacteria, molds and their products. "Stachybotrys chartarum suggests that effects in humans may be biologically plausible," but validation is required by extensive research before this conclusion can be drawn.
The committee reviewed epidemiologic studies in evaluating human health effects associated with damp indoor environments. It cautioned that: indoor environments are complex and subject occupants to multiple exposures; the studies often do not define what "dampness" means; they refer to "mold" without distinguishing between the types of mold humans are routinely exposed to 200 species of mold; and many studies are based on self-reporting.
Plaintiffs' 27, a Swedish article written in 2000, focuses on (1-3)-Beta-D-glucan, a structure in the cell wall of molds, some bacteria and plants. The article posits that the relation between respiratory symptoms and exposure to molds could be due to (1-3)-Beta-D-glucan. However, it states that there is no evidence that (1-3)-Beta-D-glucan is an allergen by the inhalation route. Allergy to the mold cell is "well known but a rare condition in a population sample," but there is good evidence that people with a preexisting allergy are particularly sensitive to (1-3)-Beta-D-glucan, which may cause an inflammatory response.
Defendants' E, The medical effects of mold exposure, the position paper of the American Academy of Allergy Asthma and Immunology, published in February 2006 in the Journal of Allergy and Clinical Immunology, reviews the state of the science of mold-related illness and what is supported by scientific evidence.[FN7] The paper makes the following observations:
Current studies do not conclusively demonstrate a causal relationship of airborne mold exposure to clinical manifestation of allergic rhinitis;
Studies attempting to correlate indoor molds to symptomatic allergic rhinitis
are problematic because of lack of quantitative mold sampling and inclusion of upper respiratory tract infections;
There are no publications that establish a causal role for airborne molds to atopic dermatitis;
Patients with allergic asthma, allergic rhinitis and atopic dermatitis commonly have IgE antibodies to molds as part of polysensitization;
Allergic responses to inhaled mold antigens are a recognized factor in asthma; [*16]
Currently available studies do not conclusively prove that exposure to outdoor airborne molds plays a role in allergic rhinitis, and studies on the contribution of indoor molds to upper airway allergy are even less compelling;
Exposure to airborne molds is not recognized as a contributing factor in atopic dermatitis;
Patients with a suspected mold allergy should be evaluated by means of an
accepted method of skin or blood testing for IgE antibodies to appropriate mold antigens as part of the clinical evaluation of potential allergies; and
Data supporting the role of fungi in chronic rhino sinusitis, are lacking at this time.
In regard to mycotoxins, the paper stated: only certain mold species produce specific mycotoxins under specific conditions; the mere presence of mold does not mean that mycotoxins are being produced; for there to be a toxic effect, the toxin must be present, there must be a route of exposure and the person must receive a sufficient dose to have a toxic effect; the main route of exposure in the non-occupational setting is inhalation; mycotoxins are not cumulative and have half-lives ranging from hours to days; and it is highly improbable that home or office mycotoxin exposure would lead to a toxic adverse health effect.
The authors state that they agree with both the statement of the American College of Occupational and Environmental Medicine and the draft of the Institute of Medicine which conclude that the evidence does not support the contention that mycotoxin-mediated disease occurs through inhalation in nonoccupational settings. The paper further disagrees with the contention that the presence of mycotoxins gives rise to a panoply of nonspecific complaints, since this would be inconsistent with what is known to occur a toxic dose creates a specific pattern of illness seen for specific mycotoxins.
The paper addresses the issue of irritant effects of mold exposure. It defines an irritant as a material causing a reversible inflammatory effect at the site of contact and notes that such an effect is transient. The paper states that MVOC levels measured in damp buildings are so low that exposure would not be expected to cause irritation in human subjects. Moreover, it recounts that individuals exposed to airborne concentrations of between 215,000 and 1,460,000 mold spores per m to the 3rd degree at work, showed no differences in respiratory symptoms at work or when on vacation. The paper states: "It should be emphasized that irritant effects involve the mucus membranes of the eyes and upper and lower respiratory tracts and are transient so that symptoms or signs persisting weeks after exposure and those accompanied by neurologic, cognitive, or systemic complaints (e.g., chronic fatigue) should not be ascribed to irritant exposure."
Finally, the paper concludes that: testing for antibodies to mycotoxins is not scientifically validated and should not be relied upon; bulk, surface and within-wall cavity measurement of molds or mycotoxins cannot be used to assess exposure; and measurement of spores are no substitute for measuring mycotoxins directly.
Defendants' F, Double blind placebo controlled exposure to molds: exposure system and clinical results, a 2005 Danish article, reports on a study of three water-damaged schools and [*17]eight employees with positive histamine release tests to Penicillium chrystogenum, who were exposed double blinded to either a placebo or one of two high concentrations of mold for six minutes per day for three days. The study found that exposure to the molds induced no more reactions than exposure to the placebo.
Defendants' G, Are indoor molds causing a new disease?, by Dr. Abba I. Terr, suggests that studies attempting to link mold to building-related illness, are not scientifically valid due to faulty methodology and insufficient data.
Defendants' H, Adverse Human Health Effects Associated with Molds in the Indoor Environment is an October 2002 evidence based position statement of the American College of Occupational and Environmental Medicine of the Council on Scientific Affairs.[FN8] It begins by noting that fungi are ubiquitous in all environments and exposure to them and their spores is unavoidable. It further notes that 10% of the population have allergic antibodies to mold, but only 5%, over a lifetime, show clinical symptoms. Moreover, the article comments that: outdoor molds are more abundant than indoor molds; allergic responses are most commonly experienced as allergic asthma or allergic rhinitis (hay fever); most fungi generally are not pathogenic to healthy humans; persons with impaired immune function are at risk for fungal infection; only some fungi are capable of producing mycotoxins; and "[c]urrent scientific evidence does not support the proposition that human health has been adversely affected by inhaled mycotoxins in the home, school, or office environment."Defendants' I, Risk from Inhaled Mycotoxins in Indoor Office and Residential Environments, published in 2004 in the International Journal of Toxicology, notes that epidemiologic evidence has not established a causal relationship between indoor mold and nonallergenic, toxigenic health effects. The article, therefore, models a maximum possible dose of mycotoxins that could be inhaled in 24 hours of continuous exposure to a high concentration of mold spores containing the maximum reported concentration of a number of molds. None of the maximum doses modeled were sufficient to cause any adverse effect. The authors surmise that delivery of mycotoxins through inhalation of mold spores is inefficient and that there is a lack of association between mold exposure and mycotoxicoses in indoor environments. The article concludes that human mycotoxicoses is "implausible following inhalation exposure to mycotoxins in mold-contaminated home, school, or office environments." And, "[u]nder the exposure conditions commonly encountered in a visibly moldy indoor environment, the potential for inhaling a toxic dose of mycotoxins is remote."
Defendants' J, Health Effects of Mycotoxins in Indoor Air: A critical Review is a 2000 review report which focuses on the toxic effects of molds associated with the production of mycotoxins and the putative association between indoor mycotoxin exposure and health. Dr. Gots was one of the authors of this paper. The article surmises that the available literature does not provide compelling evidence that exposure at levels expected in most mold-contaminated indoor environments is likely to result in measurable health effects.
Defendants' K, is an article which focuses on Stachybotrys, a species of mold not relevant to this case. [*18]
Defendants' L, is a 1992 Finnish study which looks at the effects of everyday activity on the level of fungal spores in the home.
Defendants' M, is a 2002 examination of thousands of fungal indoor and outdoor air samples to determine where and when fungal levels were highest and which fungi were most culturable.
Defendants' N, is a study of pollen and fungal spore aerobiology and speaks to measuring fungal biomass.
Defendants' O, is a 2003 review of literature regarding buildings in which occupants had no health complaints but the buildings had indoor ambient air fungal concentrations above the amount recommended for remediation. The article found that fungal concentrations in these buildings were higher than in buildings with complaints of nonspecific health symptoms.
Defendants' P, studied the reliability of using surface dust to evaluate fungal contamination.
Defendants' R, is a 2003 review of studies by a number of medical doctors and scientists to evaluate the efficacy of testing to determine the presence of IgE and IgG to specific fungi in a clinical setting. The article finds that the "ubiquitous nature of many fungi and the lack of specificity of fungal antigens limit the usefulness of these types of tests in the evaluation of potential building-related illness and fungal exposure." It concludes that there is not enough scientific evidence to support the routine clinical use of immunoassays.
Defendants' U, is a 1999 study which investigated the amounts of VOC's and MVOC's which would contribute to irritation symptoms in the upper respiratory system and eyes of people. It states that the combination of MVOCs that have been measured in the air of indoor environments are not high enough to produce irritant reactions in humans.
D. Hearing Testimony
Four witnesses testified at the hearing Dr. Paul Ehrlich, a pediatrician specializing in asthma and allergy; Dr. Eckardt Johanning, a doctor/researcher specializing in occupational and environmental medicine; Dr. Ronald Gots, a doctor/researcher specializing in forensic medicine and involved in environmental and occupational research; and Dr. Stanley Michael Phillips, director of clinical allergy and immunology services at the University of Pennsylvania Medical School and senior scholar, clinical epidemiologist and consultant of medicine at the Philadelphia Veterans' Administration Center.
1. Dr. Ehrlich
Dr. Ehrlich testified that he was a clinician, not a researcher, who specializes in pediatric allergy and asthma. He explained that an allergy occurs when a person's immune system reacts against otherwise innocuous substances. He testified that immunoglobulin IgE is produced by allergic individuals when confronted with specific substances, causing the release of histamine - an allergic reaction, i.e., runny nose, watery eyes, asthma, etc. Dr. Ehrlich testified that an IgE reaction could be "systemic," a term he failed to define. He further testified that the presence of IgE or IgG antibodies does not necessarily indicate any disease and that the most reliable test for identifying allergens is the skin prick test.
Dr. Ehrlich stated that, as an allergist, he has patients in his practice who develop reactions to damp environments, since damp buildings predispose an area to become infested with dust mites, cockroaches, molds, bacteria, proteins from animals in the environment and [*19]other things. Atypical molds will give off "toxins" or irritants. Patients with a predisposition to developing allergies are allergic to these toxins.
Dr. Ehrlich opined, based on seeing patients for 27 years, the histories they have given him and the tests and examinations he has done, that people in damp environments could develop upper and lower respiratory problems, including asthma, and may continue to have problems after being taken out of the environment when they come into contact with even small amounts of the allergens.[FN9] Dr. Ehrlich also opined, "if there are allergies, if the patient is genetically predisposed to having allergies and these allergens grow within this bad environment or this wet environment or this toxic environment, patients could conceivably have an allergic reaction." He further testified, that fatigue is a huge problem among his patients based upon the histories they have given him. The fatigue is caused by sleep problems.
2. Dr. Johanning
Dr. Johanning, a family practitioner and occupational health specialist, is a clinician involved in the treatment of patients complaining of health problems who have a reported history of exposure to indoor moisture and mold. He has been involved in the field of bioaerosols and writes on the issue of mold contamination, as well as testifies in courts throughout the country on the subject.
Dr. Johanning testified that there are guidelines in place, which he helped develop, regarding indoor mold, moisture problems and unsanitary conditions and that the "medical idea" that damp, unsanitary buildings could cause adverse human health effects was not a novel scientific concept but has been accepted science since the 1960's. In fact, he testified that moisture and mold in indoor settings has been generally known to cause adverse health effects since Biblical times and that his mother knew about it.
Citing to the studies introduced by plaintiffs into evidence, Dr. Johanning testified that moisture and mold growth in buildings can cause upper and lower respiratory problems, cough, shortness of breath, rashes, fatigue, eye problems, asthma, allergic lung diseases, intestinal problems, taste and smell disorders, neurological and cognitive problems and fatigue. He stated, "Essentially, it's recognized by the people in the field that excessive moisture leads to microbial contamination, i.e., fungi and bacteria, atypical unsanitary condition[s], that then in turn can lead, probably most often frequent cases [sic] initially to irritative type problems."Dr. Johanning defined irritative problems as transient in nature. However, he testified that with repeated exposure, an individual may develop an allergy.
Dr. Johanning stated that what is found in a damp building depends on the type of building materials used and the type and amount of water that invaded the building. The mold may or may not get airborne, depending on the type of mold, its proliferation phase and whether it dries. When inspecting a damp environment, Dr. Johanning testified, it was important to compare the amount and types of mold in the outdoor air to that in the indoor area, to see if the [*20]mold is visible, to search for abnormal signs of water entry and to observe if there is an odor. Fungi produce beta-glucans, which are part of the cell lining and an irritant. The mildew smell in damp buildings comes from high concentrations of microbial organic volatile compounds. Beta-glucans, microbial organic volatile compounds, endotoxins produced by bacteria, dust mites and cockroaches are all found in damp environments. Dr. Johanning opined that there is a strong causative correlation between allergic rhinitis and exposure to atypical molds, bacteria, endotoxins, glucans and other by-products from unsanitary microbial contamination. He also testified that it is generally accepted medical knowledge that when one recovers sample tissue from the nasal cavity of people with significant mold exposure, fungi will be found.
Describing the approved method for measuring mold, Dr. Johanning stated: Mold is collected from the air, cultured in agar and identified, and colony forming units per cubic meter of air ("CFU") is measured. Mold may also be measured by bulk sampling - taking a piece of material that looks contaminated or is implicated in some way and having that inspected for concentration of mold per square inch or per square cubic meter. Dr. Johanning testified that he has known Mr. Olmstead since 1988 and has both worked with him and co-authored papers with him. It was Dr. Johanning's opinion that the methodologies used by Mr. Olmstead in this case were in accordance with the current state of the art and guidelines in the occupational medicine and industrial hygiene fields. According to Dr. Johanning, fatigue in allergy sufferers is related to endocrine and nervous system issues.
Dr. Johanning used differential diagnosis in evaluating the Frasers, a technique, he admitted, that was not the same as a causal assessment of their complaints. In finding the Frasers' complaints caused by their damp apartment and mold, Dr. Johanning used a "more likely than not" standard. He performed blood tests, not skin prick tests, and based his diagnoses to a great degree on IgG and IgE readings.[FN10]
Dr. Johanning discounted plaintiffs' 23, the review report published by the Institute of Medicine of the National Academies at the request of the Center for Disease Control and in accordance with the guidelines of the National Research Council's Report Review Committee. Although he testified that the report was written by a panel of selected scientists with strong academic credentials who were interested in public health and that it was headed by Dr. Harrisberg, a former Harvard University faculty member, he claimed that the panel was not qualified for this study since only one person on it was a physician, it relied upon epidemiological studies rather than clinical evaluations of individual patients and it was a "theoretical", not a "pragmatic," report. He further testified that there are doctors/scientists who disagree with the report but could cite no papers to that effect. Similarly, when confronted with specific articles in Plaintiffs' 8 and 9, books he edited, he disagreed with many of them.
3. Dr. Gots
Dr. Gots, a medical doctor and Ph.D. in pharmacology, practiced emergency and occupational medicine until about 1980 and did toxicological research. He now practices forensic medicine, is involved in mold litigation and often testifies as a medical expert at trials on behalf of defendants. He also heads a company which provides litigation support.
Dr. Gots testified that certain molds can produce infection in immuno-compromised [*21]individuals and can cause allergic responses in people who are allergic to mold. However, he testified that most allergies were related to common outdoor molds and that it was unsettled if indoor mold can produce allergy, stating that it was more likely that this was true for children. Further, he testified that there was no scientific evidence that mycotoxins in indoor environments can produce disease and strong proof that it could not. He did concede that there may be some irritant effects associated with some volatile organic compounds associated with mold or mold itself.
Dr. Gots testified that not all peer-reviewed papers are reliable. Data is not checked and there may be errors in interpreting the data. In addition, the personal opinion of the author may impact on the paper's conclusions, some journals are better than others and some journals are created to promote the topic in which the paper is published. In a like manner, Dr. Gots testified, studies should be randomized and there should be a proper control group. Questionnaire information can be problematic.
Dr. Gots further testified that Dr. Johanning did not list a diagnosis in A1, A2 and A3, his medical reports of the Frasers, but instead merely listed symptoms. He stated that a differential diagnosis is not a causal assessment, but a medical process wherein a doctor evaluates symptoms and treats a disorder but does not discover the cause. He asserted that a differential diagnosis is used in the clinical setting in order to treat patients and is different from knowing something with reasonable scientific probability. In order to discover the cause of a disorder, Dr. Gots testified, one must do a causation analysis and one must have a diagnosis to do so. He explained that causation may be proved through well-designed epidemiological studies a number of studies which have consistent, statistically significant, coherent and robust results demonstrating a cause and effect between an exposure and an outcome. Causation is different from an association.
Dr. Gots continued by stating that for an airborne disease there must be an identified exposure that, if sufficient, will cause the disease - a dose response relationship. When sampling the air for mold, Dr. Gots testified, two samples taken in one day are not sufficient since the mold in air changes over time, depending on the season and weather and depending on the activity in the area. Thus, if there is snow on the ground, the level of outdoor mold will be low. Similarly, if it is raining and the wind is blowing, the level of mold will be high. A single sample taken in a short time will not be accurate.
Moreover, Dr. Gots testified that looking for antibodies in the blood is not a good way to test for mold allergy. He stated that the best method for testing for allergy to mold is skin-prick testing.
In speaking to the various exhibits introduced, Dr. Gots testified that Exhibits 21 and 27 indicate that if there is an endotoxin (various agents derived from cell walls, bacteria, etc.) exposure through inhalation, inhalation of beta glucan will not produce an inflammatory response. He also testified that there are molds and beta glucans in everyone's home and that VOCs, which are created by automobile exhaust, cleaning fluids, fireplaces and stoves, are all around us. Moreover, he explained that Exhibit E states that MVOCs (volatile organic compounds produced by mold) measured in damp buildings are usually at a level so low that exposure to them would not be expected to cause complaints of irritation in people.
4. Dr. Phillips
Dr. Phillips, a professor of medicine in Pulmonary and Allergy Critical Care, director of [*22]clinical allergy and immunology and senior clinical epidemiologist and consultant at the University of Pennsylvania Medical School, testified that he, presently, spends the vast majority of his time in clinical medicine, but has been doing research in basic immunology for twenty-five years. He further testified that many of his patients have allergies and that he sees three to four patients every day with medical issues related to mold.
Dr. Phillips testified that the cornerstone for treating patients in a clinical setting and understanding the medicine is epidemiological research. Epidemiology is the observation of a large number of people in an objective and unbiased manner to learn general principals about a particular problem. Specifically, a scientific study is designed, the population is divided into two groups - a control group and another group data from the population studied is gathered and analyzed and conclusions are drawn. Valid conclusions regarding causation cannot be made in the absence of data, since scientific method adheres to the NULL hypothesis which states that if one cannot prove something is true, one cannot conclude it is true.
Dr. Phillips testified that an association is not sufficient for a clinician to draw a conclusion about causation. He explained that an association means that two events tend to occur together. A strong association means that the association occurs all of the time, but depending upon how one looks at the problem or asks the question, it may not be a valid observation. Dr. Phillips offered two examples to illustrate this concept: 1) If one is walking down the street and sees a man in a dark suit hit by an automobile and then in the following weeks, sees other men in dark suits hit by automobiles, an association would exist between men in dark suits and pedestrian auto accidents; 2) similarly, if one were to look at cars and observe that all cars have ashtrays, a strong association would exist between cars and ashtrays. Neither observation, however, would be sufficient to come to a conclusion of causation - that only men in dark suits get hit by automobiles or that ashtrays make cars work without further studies looking at the issue from different perspectives and using a control group.
Dr. Phillips also explained the difference between review papers and research papers. A research paper provides primary data upon which a conclusion will ultimately be based. Review papers look at as many research papers as possible and evaluate their validity, relevance to the question asked and the data gathered. Thus, review papers will assess a research paper for, inter alia, its hypothesis, its design, how the data was collected, its bias if any, its size, the relation of its data to the conclusion drawn, the journal in which it was published and the prestige of the group reviewing the paper. A self-reporting population is viewed with extreme suspicion, since it has empirical bias. The patient is asked for some information in a leading manner and disproportionately is made up of individuals who are the most vocal and most salient in the population.
Commenting on the American Academy of Allergy Asthma and Immunology's position paper (Defendant's E in evidence), Dr. Phillips testified that the group was the largest and most respected group of clinical and basic allergy immunologists in the United States. He explained that a special committee of the best experts in the field of mold illness was appointed, asked to review the literature in the field and instructed to draw up a consensus statement on what molds can do in the environment. The committee's conclusions were published in 2006 and are the state of the art knowledge in the field. Dr. Phillips opined that the report was "excellent," "accurate" and in keeping with his experience. In fact, he testified that his Journal Club at the [*23]University of Pennsylvania School of Medicine reviewed the report and all of its members agreed with it. Similarly, commenting on the Institute of Medicine (the author of Plaintiffs' 23 in evidence), Dr. Phillips described the group as prestigious and as being charged with the role of "watchdog" over many medical issues and controversies in the United States.
Dr. Phillips testified that antibodies in the blood tell us that the immune system has reacted to something and has produced immunoglobulin in the past. It indicates an exposure, but does not imply a clinical disease. Antibodies, moreover, cannot tell us where the exposure took place, the amount of the exposure or when it took place.
IgE antibody is related to allergies, but IgG is not, although IgG can contribute to asthma. IgG measurements are meaningful only if there is clinical documentation of diseases which might be caused by the IgG. Even though the half-life of IgE is 3 days and that of IgG is 22 days, antibodies are replaced by new antibodies and the net effect is a long immune response. As a result, antibodies may remain in the blood for many years. It is highly unlikely that IgE would disappear from the blood in two or three years.
IgE may be measured in blood serum by doing a RAST test. Once the antibody is found in the blood, a skin prick test is done to see if there is an allergy - a clinical problem. In a skin prick test, a small amount of the allergen is injected into the skin. If a hive appears, it indicates that an allergy exists. Skin prick tests are more sensitive than blood tests, correlate better to allergy and are more clinically relevant.
In regard to IgG, Dr. Phillips testified that many people have IgG antibodies to mold and that IgG mediated symptoms must be correlated to a patient's clinical symptoms. Further, he testified that the type of IgG testing done in the Fraser case by Dr. Johanning was "very sensitive," will find IgG in everyone tested and has no clinical value.
In regard to mold, Dr. Phillips testified, 10% of individuals have antibodies to it, but only one-half of those exposed will have clinical problems.[FN11] In healthy individuals with mold allergy, symptoms of nasal congestion, itching and sneezing will be short-lived. Moreover, to test for mold in an indoor environment, there must be at least three days of sampling and careful control of the atmosphere - no heating or air-conditioning and closed windows and doors. The fewer organisms found, the more inaccurate will be the result since statistical accuracy is determined by the square root of the result.
He testified that allergists do not test for bacteria. If there is excessive moisture there probably is bacteria growth. However, the majority of bacteria do not produce endotoxin. Also, the majority of studies show where there is a lot of bacterial growth, there is less allergy. This is called the environmental hypothesis, and it says that if the immune system is turned on by responses to bacteria and endotoxin, it is turned off to allergy. Thus, the dirtier the environment, the less likely that allergy is present.
Turning to the instant plaintiffs, Dr. Phillips testified that Colin Fraser's IgE was normal, that nothing in Colin's tests showed hypersensitivity - a strong reaction to material causing clinical symptoms and that the tests done were not compatible with hypersensitivity. As to Pamela Fraser, Dr. Phillips testified that the only IgE response she had was to dust. According to [*24]him, this test is no longer done by allergists since the dust used is a mix from 200 vacuum cleaner bags containing many different components. He also stated that her medical records indicated a cat allergy, and testified that no testing for allergies was done on Alexandra Fraser since she was too young. Finally, he testified that the Olmstead report's colony counts were "incredibly low," lower than those found in a normal home. He described the Fraser apartment as a very clean environment which fell within public guidelines in terms of acceptable levels of mold contamination.
5. Court's Credibility Findings
The court found Dr. Johanning and Dr. Gots far from objective. Both men appeared to have strongly held views on the subject of mold and a stake in advancing those views. Further, Dr. Johanning's opinions were not in keeping with the bulk of the scientific literature and often were discredited even by articles he himself had edited or written. Moreover, his testimony was based on clinical, differential diagnosis in individual cases, and he specifically discounted published studies by epidemiologists, scientists and well-regarded institutions, because they were not written by clinicians.
Dr. Ehrlich, though credible, is a clinician, not a researcher. His testimony about allergy to mold was based upon his observations of individual patients and their histories. I credit his testimony as to the general concepts of allergy, but do not find him to be an expert in epidemiology or the causation of disease, if any, by mold or a damp environment. Finally, I found Dr. Phillips credible, knowledgeable and very impressive. Accordingly, based on the credible testimony of the witnesses and the scientific literature introduced, I make the following findings.
II. Conclusions of Law
In determining the admissibility of questioned expert testimony at trial, New York continues to adhere to the traditional standard as explicated in Frye v. United States, 293 F. 1013 (D.C. Cir. 1923). People v. Wesley, 83 NY2d 417, 424, n.2 (1994)(Court specifically stated Daubert v. Merrill Dow Pharms., Inc., 509 U.S. 579 (1993) standard was not applicable in New York).[FN12] The Frye Court noted that "when a scientific principle or discovery crosses the line between the experimental and demonstrable stages . . . the evidential force of the principle must be recognized, and while courts will go a long way in admitting expert testimony deduced from a well-recognized scientific principle or discovery, the thing from which the deduction is made must be sufficiently established to have gained general acceptance in the particular field in which it belongs." From this discussion grew the oft-cited Frye test - an expert may testify regarding [*25]novel scientific principles, procedures or theories if they have gained general acceptance in the relevant scientific community. See People v. Wernick, 89 NY2d 111, 114 (1996); Nonnon v. City of New York, 819 NYS2d 705, ___A.D.3d___ (1st Dept. 2006) ; Zito v. Zabarsky, 28 AD3d 42 (2d Dept. 2006).
In applying the Frye standard, New York courts have recognized that there need not be unanimity in the relevant scientific community to permit admission, acknowledging that the basis for the rule is reliability. Wesley, supra , citing to People v. Middleton, 54 NY2d 42, 49 (1981). Accord Lewin v. County of Suffolk, 18 AD3d 621, 622 (2d Dept. 2005)(where no scientific organization or national board had expressly recognized plaintiff's theory and peer-reviewed scientific articles and textbooks relied upon by plaintiff's experts did not establish causal relationship, expert's testimony was "fundamentally speculative" and inadmissible); Pauling v. Orentreich Med'l. Group, 14 AD3d 357 (1st Dept.), lv. denied 4 NY3d 710 (2005)(plaintiff failed to meet burden of proof at Frye hearing where no medical literature submitted to support theory and no scientific or medical board recognized causal relationship); Marsh v. Smyth, 12 AD3d 307 (1st Dept. 2004)(Frye test met where expert's deductions were supported by medical literature); Saulpaugh v. Krafte, 5 AD3d 934 (3d Dept.), lv. Denied 3 NY3d 610 (2004)(broad statement of scientific acceptance without accompanying support, insufficient to establish scientific acceptance of theory); Lara v. N.Y.C. Health and Hosp. Corp., 305 AD2d 106 (1st Dept. 2003)(Frye test not met where no reported medical cases or formal studies supported theory); Selig v. Pfizer, Inc., 290 AD2d 319 (1st Dept.), lv. Denied, 98 NY2d 603 (2002)(where clinical data did not support expert's theory of causal link and expert failed to set forth other scientific evidence based on accepted principles to support causal link, expert precluded). The proponent of the novel science bears the burden of demonstrating its admissibility. Lewin, supra ; Pauling, supra ; Saulpaugh, supra ; Lara, supra . Here, plaintiffs have failed to carry their burden.
The sole expert to testify that mold and/or damp indoor space causes health problems was Dr. Johanning.[FN13] However, the scientific literature introduced did not support his assertions. Instead, the two scientific documents found most compelling by the court - the Institute of Medicine of the National Academies' 2003 publication (Plaintiffs' 23) and the 2006 position paper of the American Academy of Allergy Asthma and Immunology (Defendant's E) - found no causative link. These two papers were issued by prestigious scientific organizations and, most important, reviewed the available research papers on the subject for validity, a task far beyond the capability of this court. The papers concluded that there was insufficient evidence to support the contention that a causal relationship exists between health outcomes and damp and/or moldy indoor environments. Indeed, the American College of Occupational and Environmental Medicine, the governing body of Dr. Johanning's specialty, issued a formal position paper coming to the same conclusion - "scientific evidence does not support the proposition that human health has been adversely affected by inhaled mycotoxins in the home, school, or office environment." The bald statements of Dr. Johanning, unsupported by the scientific literature and refuted by both Dr. Phillips and three distinguished bodies influential in the field of immunology and occupational health, do not meet the Frye standard. See Lewin, supra , 18 AD3d 622; [*26]Pauling, supra , 14 AD3d 357; Marsh, supra , 12 AD3d 307; Saulpaugh, supra , 5 AD3d 934; Lara, supra , 305 AD2d 106; Selig, supra , 290 AD2d 319.
This standard is not met, as Dr. Johanning would have us believe, by anecdotal or individual case studies. Nor is it met by the more likely than not standard he puts forth. Rather, Frye requires that plaintiffs prove that causation of illness by mold and/or damp indoor environments is generally accepted by the relevant scientific community. Here, plaintiffs failed to demonstrate that the community of allergists, immunologists, occupational and environmental health physicians and scientists accept their theory - that mold and/or damp indoor environments cause illness.
In addition, even were there a showing of causation here, this case could not go forward. It became clear at the hearing that plaintiffs wished to argue that moisture in the Fraser apartment caused them ill health. Plaintiffs contended that a damp indoor environment produced bacteria, mold, endotoxins, Beta Glucans, MVOCs and other toxic materials, which caused the Frasers' complained of symptoms. However, moisture, bacteria, endotoxins, MVOCs and Beta Glucans were never measured in the Fraser apartment. Moreover, the scientific literature and the testimony of Dr. Phillips established that two measurements for mold in a short time span, the method of measurement used here, was insufficient to give a valid mold reading. Then too, the hearing evidence demonstrated that: there are no standards for what amount of mold was excessive in terms of human health and the indoor environment; there are no generally accepted standards for measuring indoor airborne mold; there are no generally accepted standards for the acceptable amount of mold in indoor air; there are many types of mold, each of which have different or no health effects; there are no standard scientific definitions for "dampness" or "moisture"; skin prick tests for allergy, which were not done here, were deemed the most reliable way to test for allergy by the literature, Dr. Ehrlich, Dr. Gots and Dr. Phillips; and the IgE test performed on Colin and Pamela Fraser, which is related to allergies, did not show allergy to mold. Accordingly, it is
ORDERED that plaintiffs are precluded from introducing testimony demonstrating that mold caused their health complaints and plaintiffs' causes of action based upon personal injury are dismissed with prejudice; and it is further
ORDERED that the remaining causes of action are severed and shall continue; and it is further
ORDERED that the parties are directed to appear in Part 54, Supreme Court, New York County, on October 12, 2006, for a status conference.
DATED September 27, 2006____________________________