Airborne fiberglass dust hazards & the role of particle size in particle detection as well as in health risk assessment:

Most buildings Probably have Mostly Large Fiberglass Fragments. Prudent Avoidance of Fiberglass Insulation Dust makes sense.

This article provides information about fiberglass fragments and indoor air quality fiberglass contamination issues in residential and light-commercial buildings.

Airborne Fiberglass Fragments as a Possible Health Concern

A Guide to Large versus Very Small Fiberglass Fragments in Building Dust

In our page top photo of fiberglass insulation fragments collected in an indoor air sample, you can see not only a large and typical fiberglass insulation strand with its characteristic colored resin binder. You can also spot much smaller fiberglass fragments.

When a forensic laboratory is asked to screen dust or air samples for fiberglass, depending on the lab's protocols it's not certain that fibers of both large dimension and small fiber fragments will both be reported.

Small glass fiber fragments are easily "lost" in other non-fungal granular debris in building dust. We posit that studies of the level of airborne fiberglass in buildings may be faulty if the methods used to screen for fiberglass fragments do not include small, even sub-micron particles along with the common large particles.

Most buildings Probably have Mostly Large Fiberglass Fragments - Some Have Sub-Micron Fragments of Fiberglass Dust

Our field and lab experience suggest that while we find fiberglass in nearly all modern indoor environmental dust, the common particles are usually long and large (and presumed less of a health risk than very small particles).

However in environments where fiberglass insulation is old, damaged [photo] by foot traffic, handling, pests such as mice, or where it was chopped or disturbed, on occasion we find high levels of very small, even sub-micron fiberglass particles.

We may also find an elevated level of small fiberglass insulation fragments in buildings or in the HVAC system of buildings where fiberglass-lined HVAC ductwork has been mechanically cleaned [photo] - a process that can loosen and damage the fiberglass liner.

We have also found high levels of fiberglass fragments in indoor air and dust in buildings where amateur do-it-yourself return air ducts were constructed using conventional fiberglass insulating batts as a "duct" liner (photo, above-left).

Therefore a first level of inspection for this hazard starts with the age of the building and the visual determination of the condition of its insulation.

Fiberglass fragments are inorganic material typically from fiberglass insulation; depending on their size and quantity these may be a respiratory irritant or may contribute to more serious health concerns.

The presence of incidental occurrence of fiberglass fragments and fibers in buildings is common.

The Association of Man-made Mineral Fiber Producers asserted to the US EPA in 1992 that a study at that time " does not provide evidence of significant adverse health effects following inhalation of glass fiber."

("Respirable Fibrous Glass Chronic Multidose Inhalation Study-Preliminary Final Results," TIMA, 4 May 1992 delivered to U.S. EPA by hand.) The Seventh Annual Report on Carcinogens (June 1994) lists glass fibers of respirable size as a substance "reasonably anticipated to cause cancer in humans."

DJF Opinion: Caution about fiberglass fragment size: when reading studies about airborne fiberglass, pay close attention to the methods used to collect samples and the methods used to identify and count fiberglass particle fragments.

For example, some counting devices or microscopic methods exclude all particles below a give size by the choice of instrument or counting method itself.

See LAB IDENTIFICATION OF FIBERGLASS for details.

Deciding not to look for very small particles (which if present may be the more harmful ones) or using a methodology that excludes them means that study is not going to find them even if they in fact were dominant by number or even total volume in a sample.

Prudent Avoidance of Fiberglass Insulation Dust

It is possible that small fiberglass particles in air may constitute a meaningful health risk (obviously depending on the overall exposure level) which has not been explored. It seems reasonable to me to suggest that that prudent avoidance of fiberglass dust would be appropriate.

Improper cleaning or treatment of fiberglass ducts with biocides and particularly, mechanical cleaning that can damage the fiberglass lining HVAC ducts may in fact increase rather than decrease indoor air quality problems in a building, particularly if occupants have other respiratory or pulmonary concerns/vulnerabilities.

See Glass Wool Fibers Expert Panel Report, Part B - Recommendation for Listing Status for Glass Wool Fibers and Scientific Justification for the Recommendation" [PDF] for a 2009 update on the carcinogenicity of fiberglass fragments.

Following a discussion of the body of knowledge, the expert panel reviewed the RoC listing criteria and made its recommendation.

The expert panel recommended by a vote of 8 yes/0 no that glass wool fibers, with the exception of special fibers of concern (characterized physically below), should not be classified either as known to be a human carcinogen or reasonably anticipated to be a human carcinogen.

The expert panel also recommended by a vote of 7 yes/0 no/1 abstention, based on sufficient evidence of carcinogenicity in well-conducted animal inhalation studies, that special-purpose glass fibers with the physical characteristics as follows longer, thinner, less soluble fibers (for 1 example, > 15 μm length with a kdis of < 100 ng/cm2/h) are reasonably anticipated to be a human carcinogen for the listing status in the RoC.

The major considerations discussed that led the panel to its recommendation include the observations of tumors in multiple species of animals (rats and hamsters). Both inhalation and intraperitoneal routes of exposure produced tumors, although inhalation was considered more relevant for humans.

Reader Question: exposure to airborne fiberglass & VOCs from fiberglass boat manufacture

19 March 2015 Anonymous said:

I have a related question as well, i work in a an area where we are on a second floor and on our ground floor, is our production area, wherein the polish a fiber glass boat.

My concern is when our AC is open, Is the fiber being suck up by our AC wherein we get to inhale the fiber? At the same time, we can even smell the resin, is this dangerous to our health??

Reply: OSHA Workplace Safety Forms

Anon

This is an OSHA workplace safety question for you and your company's safety officer, and in my OPINION a valid one, and not one for which the actual risks can be assessed by an e-text. Rather an onsite inspection by an expert would be needed.

If you need help from OSHA and the U.S. Department of Labor, see:

• The OSHA Whistleblower Protection Programs - http://www.whistleblowers.gov/
• OSHA Online Whistleblower Online Complaint Form - https://www.osha.gov/whistleblower/WBComplaint.html
• Download the Notice of Whistleblower Complaint Form (OSHA 8-60.1) [PDF] - this form is then mailed to your
  
  
  OSHA Regional Office - http://www.osha.gov/html/RAmap.html
  
  You can also call your regional OSHA office directlyi with questions, locating your office from the link we've just given or you can mail a letter to your OSHA local or reginal office.

While no one can assess risks in your workplace by just a text inquiry, it is reasonble to say that it is possible for particles and gases to be transported from one building area to another by an HVAC system, more-so if its filtration is not designed for the tansk at hand. Odors from resins or chemicals used in making a fiberglass boat (styrene emissions) or for cleaning up (acetone) are quite volatile - it's no surprise that they'd spread in a building. These hazards have been investigated by experts. For example, see

• FIBERGLASS REINFORCED PLASTICS - Fiberglass Reinforced Plastics FRP - Handling, Repair & Hazard Information
• Canter, Environmental Protoection. "Assessment of VOC Emissions from Fiberglass Boat-Manufacturing." [PDF] large 3MB file, U.S. EPA, EPA-600/2-90-019, May 1990.
  Excerpts from the reporty abstract:
  
  This report presents an assessment of VOC emissions from fiberglass boat manufacturing. ... VOC emissions from this industry consist mainly of styrene emission from gel coating and lamination, and acetone or other solvent emissions from clean-up activities.
• Guo, Jie, Ying Jiang, Xiaofang Hu, and Zhenming Xu. "Volatile organic compounds and metal leaching from composite products made from fiberglass-resin portion of printed circuit board waste." Environmental science & technology 46, no. 2 (2011): 1028-1034.
• Scheffey, Joseph L., and PE Craig L. Beyer. "Preliminary Fire Hazard Analysis of Composite Resin Manufacturing Spray Application Areas." (2007).
• Kulakool, Ruttanachote. "Greener and Safer Resin Cleaning Solvent: a Surfboard Manufacturing Process." PhD diss., Mahidol University, 2007.

Research: Silicosis among Glass Workers

• Akgün, Metin, and Begüm Ergan. "Silicosis in Turkey: is it an endless nightmare or is there still hope?." Turkish thoracic journal 19, no. 2 (2018): 89.
• Azari, Mansour R., Mohammad Rokni, Sousan Salehpour, YAD ELAH MEHRABI, Mohammad Javad Jafari, MOADELI A. NASER, Mohammad Movahedi et al. RISK ASSESSMENT OF WORKERS EXPOSED TO CRYSTALLINE SILICA AEROSOLS IN THE EAST ZONE OF TEHRAN [PDF] (2009): 43-50.
  
  ABSTRACT Background: The term "crystalline silica" refers to crystallized form of SiO2 and quartz, as the most abundant compound on earth crust, is capable of causing silicosis and lung cancer upon inhaling large doses in course of occupational exposure.
  
  Materials and Methods: In this study, airborne respirable dust samples were collected on mixed cellulose filters (25 mm diameter, 0.8 mm pore size), by using a cyclone separator at the flow rate of 2.2 l/min for a maximum volume of 800 liters. Infrared absorption spectrometry was used according to the "National Institute of Occupational Safety and Health" (NIOSH) method No. 7602 for analysis of samples. Risk assessment techniques predictive of silicosis and lung cancer were employed.
  
  Results: The geometric mean of workers' exposure to crystalline silica in ten industrial fields (stone milling and cutting, foundry work, glass manufacturing, asphalt, construction, sand and gravel mining, sand blast, ceramics, bricks and cement manufacturing) was in the range of 0.132 to 0.343 mg/m3 . Mortality rate of silicosis was predicted to be in range of 1 to 52 per one thousand exposed individuals. Risk of lung cancer mortality in exposed workers in the east zone of Tehran based on geometric mean exposure of industrial activity and 45 years of exposure was in range of 50 to 129 per one thousand. In terms of risk assessment of silicosis mortality, cumulative exposure of 21 percent of population complied with the notion of acceptable risk. In regard to lung cancer mortality, 100 percent of the population were expected to have an unacceptable risk after 45 years of active work experience.
  
  Conclusion: This study is the first of its kind in Iran demonstrating a profile of exposure in different groups of workers in the east zone of Tehran's greater city, covering 5.5 million populations. Considering the total population of one hundred thousand workers exposed to quartz in east zone of Tehran and aging of the current young workforce, numerous cases of silicosis and lung cancer are forecasted in near future. (Tanaffos 2009; 8(3): 43-50) Key words: Silicosis, Quartz, Lung cancer, Risk assessment and management
• Chiazze, Leonard, Deborah K. Watkins, Cheryl Fryar, and Joseph Kozono. "A case-control study of malignant and non-malignant respiratory disease among employees of a fiberglass manufacturing facility. II. Exposure assessment." Occupational and Environmental Medicine 50, no. 8 (1993): 717-725.
  
  Abstract A case-control study of malignant and non-malignant respiratory disease among employees of the Owens-Corning Fiberglas Corporation's Newark, Ohio plant was undertaken. The aim was to determine the extent to which exposures to substances in the Newark plant environment, to non-workplace factors, or to a combination may play a part in the risk of mortality from respiratory disease among workers in this plant. A historical environmental reconstruction of the plant was undertaken to characterise the exposure profile for workers in this plant from its beginnings in 1934 to the end of 1987.
  
  The exposure profile provided estimates of cumulative exposure to respirable fibres, fine fibres, asbestos, talc, formaldehyde, silica, and asphalt fumes. Employment histories from Owens-Corning Fiberglas provided information on employment characteristics (duration of employment, year of hire, age at first hire) and an interview survey obtained information on demographic characteristics (birthdate, race, education, marital state, parent's ethnic background, and place of birth), lifetime residence, occupational and smoking histories, hobbies, and personal and family medical history. Matched, unadjusted odds ratios (ORs) were used to assess the association between lung cancer or non-malignant respiratory disease and the cumulative exposure history, demographic characteristics, and employment variables.
  
  Only the smoking variables and employment characteristics (year of hire and age at first hire) were statistically significant for lung cancer. For non-malignant respiratory disease, only the smoking variables were statistically significant in the univariate analysis. Of the variables entered into a conditional logistic regression model for lung cancer, only smoking (smoked for six months or more v never smoked: OR = 26.17, 95% confidence interval (95% CI) 3.316-206.5) and age at first hire (35 and over v less than 35: OR = 0.244, 95% CI 0.083-0.717) were statistically significant.
  
  There were, however, increased ORs for year of employment (first hired before 1945 v first hire after 1945: OR = 1.944, 95% CI 0.850-4.445), talc (cumulative exposure >1000 fibres/ml days v never exposed: OR = 1.355, 95% CI 0.407-5.515), and asphalt fumes (cumulative exposure >0.01 mg/m(3) days v never exposed: OR 1.131, 95% CI 0.468-2.730). For non-malignant respiratory disease, only the smoking variable was significant in the conditional logistic regression analysis (OR = 2.637, 95% CI 1.146-6.069).
  
  There were raised ORs for the higher cumulative exposure categories for respirable fibres, asbestos, silica, and asphalt fumes. For both silica and asphalt fumes, ORs were more than double the reference groups for all exposure categories. A limited number of subjects were exposed to fine fibres. The scarcity of cases and controls limits the extent to which analyses for fine fibre may be carried out. Within those limitations, among those who had worked with fine fibre, the unadjusted, unmatched OR for lung cancer was (1.0 (95% CI 0.229-4.373) and for non-malignant respiratory disease, the OR was 1.5 (95% CI 0.336-6.702).
  
  The unadjusted OR for lung cancer for exposure to fine fibre was consistent with that for all respirable fibre and does not suggest an association. For non-malignant respiratory disease, the unadjusted OR for fine fibre was opposite in direction from that for all respirable fibres. Within the limitations of the available data on fibre, there is o suggestion that exposure to fine fibre has resulted in an increase in risk of lung cancer.
  
  The increased OR for non-malignant respiratory disease is inconclusive. The results of this population, in this place and time, neither respirable fibres nor any of the substances investigated as part of the plant environment are statistically significant factors for lung cancer risk although there are increased ORs for exposure to talc and asphalt fumes. Smoking is the most important factors in risk for lung cancer in this population. The situation is less clear for non-malignant respiratory disease. Unlike lung cancer, non-malignant respiratory represents a constellation of outcomes and not a single well defined end point.
  
  Although smoking was the only statistically significant factor for non-malignant respiratory disease in this analysis, the ORs for respirable fibres, asbestos, silica, and asphalt fumes were greater than unity for the highest exposure categories. Although the raised ORs for these substances may represent the results of a random process, they may be suggestive of an increased risk and require further investigation.
• Enterline, Philip E., and Vivian Henderson. "The health of retired fibrous glass workers." Archives of Environmental Health: An International Journal 30, no. 3 (1975): 113-116.
  Abstract:
  
  A total of 416 men, retiring during the period 1945 to 1972 from six plants engaged mainly in the manufacture of fibrous glass insulation, were studied to see how their mortality experience compared with that of white men in the entire United States living in comparable age and time intervals. The mean follow-up period from first exposure was about 30 years.
  
  Overall mortality was low and there was no evidence of an excess in respiratory cancer mortality. No mesotheliomas were noted. For 115 men retiring from the same six plants during the period 1945 to 1972 due to a disability the distribution of disabilities by cause was compared with an expected distribution based on the experience of the Social Security Administration.
  
  This comparison showed no evidence of any unusual health hazards among fibrous glass workers, except a possible excess in chronic bronchitis.
• Goldsmith, John R., and David F. Goldsmith. "Fiberglass or silica exposure and increased nephritis or ESRD (end‐stage renal disease)." American journal of industrial medicine 23, no. 6 (1993): 873-881.
  
  Abstract The U.S. multiplant cohort mortality study of workers producing manufactured mineral fibers is finding increasing mortality from nephritis and/or nephrosis. We examine other data sets to see if similar effects can be identified.
  
  In a case‐referent study among Michigan patients with end‐stage renal disease (ESRD), men with exposures to silica have elevated odds ratio for ESRD.
  
  In a California occupational mortality study based on 1979–81 data, a number of the construction trades, farmers, and farm laborers show excess mortality for renal disease. The highest mortality ratio is found in the category including insulation workers. This ratio remains significantly elevated when adjusted for estimated exposures to smoking, alcohol, and for socio‐economic status. California mortality data from 20 years earlier (1959–61) fail to show much excess renal disease in construction workers, but do for farmers. In Singapore, granite workers with a long‐term exposure to silica have excess excretion of albumin and similar compounds compared to less exposed controls, leading to the presumption that silica exposure can lead to silica nephrotoxicity.
  
  Balkan nephropathy has been associated with consumption of well water high in silica. In the Negev of Israel, dust storms are a vehicle for increasing respiratory uptake of silica. The Beduin, thought to be a population with maximal exposures, have higher rates of ESRD than do Jews in the age groups over 60 years.
  
  Although high blood concentrations of silica are found in persons with renal failure, the close association with elevated creatinine has been interpreted as evidence that the buildup of silica is due to renal failure, rather than vice‐versa.
  
  The evidence is consistent with, but not yet compelling, that exposure to silica, which can be readily absorbed (or dissolved) from the lung, may increase the long‐term risk of renal disease including renal failure. © 1993 Wiley‐Liss, Inc.
• Greenberg, Michael I., Javier Waksman, and John Curtis. SILICOSIS: A REVIEW [PDF] Disease-a-Month 53, no. 8 (2007): 394-416.
  Excerpts:
  
  Opal, diatomaceous earth (tripolite), silica-rich fiberglass, fume silica, mineral wool, and silica glass (vitreous silica) are common amorphous forms of silica.
  
  Dusts composed of amorphous silica, with the exception of fiberglass, are not generally considered to be harmful to humans. 9 [Mossman 1998]
• Kramer, Mordechai R., Paul D. Blanc, Elizabeth Fireman, Anat Amital, Alexander Guber, Nader Abdul Rhahman, and David Shitrit. "Artificial stone silicosis: disease resurgence among artificial stone workers." Chest 142, no. 2 (2012): 419-424.
• Leung, Chi Chiu, Ignatius Tak Sun Yu, and Weihong Chen. "Silicosis." The Lancet 379, no. 9830 (2012): 2008-2018.
  
  Summary: Silicosis is a fibrotic lung disease caused by inhalation of free crystalline silicon dioxide or silica. Occupational exposure to respirable crystalline silica dust particles occurs in many industries. Phagocytosis of crystalline silica in the lung causes lysosomal damage, activating the NALP3 inflammasome and triggering the inflammatory cascade with subsequent fibrosis. Impairment of lung function increases with disease progression, even after the patient is no longer exposed. Diagnosis of silicosis needs carefully documented records of occupational exposure and radiological features, with exclusion of other competing diagnoses. Mycobacterial diseases, airway obstruction, and lung cancer are associated with silica dust exposure. As yet, no curative treatment exists, but comprehensive management strategies help to improve quality of life and slow deterioration. Further efforts are needed for recognition and control of silica hazards, especially in developing countries.
• Marinaccio, Alessandro, Alberto Scarselli, Giuseppe Gorini, Elisabetta Chellini, Marina Mastrantonio, Raffaella Uccelli, Pierluigi Altavista, Roberta Pirastu, Domenico Franco Merlo, and Massimo Nesti. "Retrospective mortality cohort study of Italian workers compensated for silicosis." Occupational and environmental medicine 63, no. 11 (2006): 762-765.
  
  Abstract :Objectives: To estimate cause specific mortality in a large cohort of Italian workers compensated for silicosis.
  
  Methods: The cohort included 14 929 subjects (14 098 men and 831 women) compensated for silicosis between 1946 and 1979, alive on 1 January 1980, and resident in Tuscany (a region of central Italy with 3 547 000 inhabitants). Mortality follow up ranged from 1980 to 1999. Vital status and the causes of death were determined by linkage with the regional mortality registry and with the national mortality database. The cohort mortality rates were compared to the rates of the local reference population. SMRs and their 95% confidence intervals were computed assuming a Poisson distribution of the observed deaths. Specific SMR analyses were performed according to the level of disability, the year of compensation assignment, and the job type.
  
  Results: A significant excess mortality was observed in male silicotics for cancer of the lung, trachea, and bronchus and cancer of the liver, respiratory diseases (silicosis, asbestosis, antracosilicosis, and other pneumoconiosis), and for tubercolosis. Statistically significant mortality excess was observed in female silicotics for respiratory diseases (specifically silicosis and other pneumoconiosis) and tuberculosis. Analyses for period of compensation assignment showed a twofold increased SMR for biliary tract cancer among female workers and for liver cancer among male workers compensated before 1970.
  
  Conclusions: The excess mortality from respiratory tract cancers and respiratory tract diseases detected in Italian compensated silicotics are in agreement with previous epidemiological studies. Although the twofold increased risk for liver cancer among males is suggestive of a possible association with silica dust exposure, the finding needs to be confirmed.
• Mossman BT, Churg A. Mechanisms in the pathogenesis of asbestosis and silicosis. Am J Respir Crit Care Med 1998;157(5 Pt 1):1666-80
• Murgia, Nicola, Giacomo Muzi, Marco dell'Omo, Domenico Sallese, Cesario Ciccotosto, Margherita Rossi, Paola Scatolini et al. "An old threat in a new setting: high prevalence of silicosis among jewelry workers." American journal of industrial medicine 50, no. 8 (2007): 577-583.
  
  Abstract Background Silicosis is caused by inhaling free crystalline silica. Few case reports have addressed the risk of silicosis in the jewelry trade where chalk molds containing a high percentage of silica are used in casting. We conducted a cross‐sectional study involving 100 goldsmiths exposed to silica.
  
  Methods All workers replied to a questionnaire and underwent a clinical examination, pulmonary function tests, a chest X‐ray and a high‐resolution CT scan.
  
  Results High‐resolution CT visualized signs of silicosis in 23 cases, confirmed by standard chest X‐rays in 10. In the 23 workers with CT evidence of silicosis Total Lung Capacity, FEV1 and the Lung Diffusing Capacity did not differ from the workers without the disease. Pulmonary function tests did not correlate with silica exposure.
  
  Conclusion In this study we demonstrate that use of chalk molds in casting in jewelry causes silicosis. The composition of the dust could be responsible of the high prevalence observed. Am. J. Ind. Med. 50:577–583, 2007. © 2007 Wiley‐Liss, Inc.
• Pérez-Alonso, Aránzazu, Juan Antonio Córdoba-Doña, José Luis Millares-Lorenzo, Estrella Figueroa-Murillo, Cristina García-Vadillo, and José Romero-Morillo. "Outbreak of silicosis in Spanish quartz conglomerate workers." International journal of occupational and environmental health 20, no. 1 (2014): 26-32.
• Vahid, Bobbak, MD., Bharat Awsare, MD., and Paul E. Marik, MD. "Respiratory Disease and Fiberglass Exposure: Report of a Case and Review of the Literature." Clinical Pulmonary Medicine 14, no. 5 (2007): 296-301.
  
  Abstract: This report describes a 23-year-old man with exposure to fiberglass who presented with dry cough of 4 months duration. Computed tomography of the chest showed mediastinal lymph node enlargement and pulmonary infiltrates. Lymph node biopsy showed granulomatous lymphadenitis with giant cell formation. The mediastinal lymphadenopathy and the pulmonary infiltrates resolved after cessation of fiberglass exposure.
  
  The effects of fiberglass exposure on the respiratory system have been evaluated in several epidemiologic studies. Although fiberglass is widely used and low levels of exposure are commonplace, these studies have not shown a significant increase in mortality from respiratory malignancies or nonmalignant respiratory diseases in individuals with fiberglass exposure.
  
  The commonly reported abnormal findings on chest radiographs are low profusion micronodular opacities, hilar enlargement, and pleural thickening. Rare cases of pulmonary fibrosis, acute eosinophilic pneumonia, and sarcoidosis-like pulmonary disease have been described after exposure to fiberglass.
  
  Detailed exposure history is essential to make the diagnosis. Cessation of fiberglass exposure is important in management of these patients. Inhalation fever, reactive airway disease, and chemical pneumonitis also can be the result of exposure to an endotoxin or binder agents.
  
  From the Department of Pulmonary and Critical Care Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania. Address correspondence to: Bobbak Vahid, MD, 834 Walnut Street Suite 650, Philadelphia, PA 19107. E-mail: bobbak.vahid@mail.tju.edu

...

Continue reading at FIBERGLASS HVAC DUCTS or select a topic from the closely-related articles below, or see the complete ARTICLE INDEX.

Or see FIBERGLASS HAZARDS in AIR or DUST FAQs - questions & answers posted originally at this article

Or see these

Articles on Fiberglass Hazards in Buildings

• FIBERGLASS HAZARDS - home
  • AIR FILTERS, FIBERGLASS PARTICLES
  • DUST ANALYSIS for FIBERGLASS
  • FIBERGLASS DETECTION in BUILDING AIR & DUST
  • FIBERGLASS ENVIRO-SCARE
  • FIBERGLASS FRAGMENT HAZARDS in AIR or DUST
  • FIBERGLASS HAZARD RESEARCH
  • FIBERGLASS INSULATION EXPOSURE LIMITS
  • FIBERGLASS PARTICLE CONTAMINATION TEST
  • FIBERGLASS REINFORCED PLASTICS
  • FIBERGLASS SHEDDING from MATTRESSES
  • FORMALDEHYDE in FIBERGLASS INSULATION
• FIBERGLASS HVAC DUCTS
• MORGELLONS SYNDROME

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