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Ozone exposure & hazard references: This article provides technical sources & references regarding the effects of using ozone in buildings for these purposes and warns consumers about misapplication of and health risks from ozone in buildings.
Ozone is widely promoted by ozone generating equipment companies and cleaning services for use in indoor
building environments to deodorize, disinfect, kill mold, and for general health.
Ozone generators are also promoted for use to reduce the level of airborne particles, pollen, animal dander, and allergens, ostensibly to improve indoor air quality for asthmatics and people with allergies.
Ozone & Ozone Treatments for Odors or Mold Contamination: References & Technical Documentation, PELS, MSDS
While there are some important uses of ozone (such as for medical disinfection under controlled conditions),
in general this is an idea which ranges from bad to dangerous in the home. Because at least some of these claims are based on marketing desire, not good science, and
because ozone exposure can be both dangerous and ineffective indoors, we have
collected some information and references on this topic.
Ozone exposure limits: NIOSH REL: C 0.1 ppm (0.2 mg/m3);
OSHA PEL: TWA 0.1 ppm (0.2 mg/m3)
 Ozone and other contaminants discussed, New York State Department of
is not a substitute for mold removal and its reaction with building materials,
but applied by an expert may help deodorize, a cleaning article by Jim Holland -
 Ozone as an oxidant, a few references from the Canadian Government
H., Campbell K. S., and Appel, W. D. (1952). The oxidation of cellulose by ozone in small
concentrations. Text. Res. J. 22: 81-83.
C. E., and Haagen-Smit, A. J. (1951). The application of rubber in the
quantitative determination of ozone. Rubber Chem. Technol. 24: 750-755.
Cass, G. R., Nazaroff, W. W., Tiller, C., and Whitmore, P. M. (1991). Protection of
works of art from damage due to atmospheric ozone. Atmospheric Environment,
25A( 2): 441-451.
Druzik, J. R. (1985). Ozone: The Intractable Problem. We stern Association for Art
Conservation newsletter. Http://sul-server-2.stanford.edu/waac/wn/wn07/wn07-3/wn07-302.html
(vol.7, no. 3)
9 "Health Hazards of some Gases" Jack E. Peterson, P.E., CIH, Ph.D., May, 1987
Sampling for gases in air such as VOC's, MVOC's, toxic chemicals, and combustion products.
Unfortunately no single test or tool can detect all possible building contaminants. We use methods and equipment which can test for common
contaminants. If the identity of a specific contaminant is known in advance we can also test for a very large number of specific contaminant
gases in buildings.
We use gas sampling equipment provided by the two most reliable companies
in the world, Draeger-Safety's detector-tubes and Drager accuro bellows pump, the Gastec cylinder pump
and detector-tube system produced by Gastec or Sensidyne, and
we also use Sensidyne's Gilian air pump. For broad screening for combustibles and a number of other
toxic gases and for leak tracing we also use Amprobe's Tif8850. All of these instruments, their applications, and sensitivities (minimum detectable limits) for specific
gases are described in our Gas Sampling Plan online document.
U.S. Clean Air Act - large PDF - epw.senate.gov/envlaws/cleanair.pdf
"Ozone-Generating Air Cleaners and Indoor Air Chemistry" , U.S. Environmental Protection Agency, original document is available at: epa.gov/appcdwww/iemb/ozone.htm
"Ozone Generators that are Sold as Air Cleaners", U.S. Environmental Protection Agency, original document is available at: epa.gov/iaq/pubs/ozonegen.html "EPA reviewed a wide assortment of this literature, including information provided by a leading manufacturer of ozone generating devices. In keeping with EPA's policy of insuring that the information it provides is based on sound science, only peer reviewed, scientifically supported findings and conclusions were relied upon in developing this document."
Association of Home Appliance Manufacturers (AHAM) 1111 19th Street, NW, Suite 402, Washington, DC 20036, (202) 872-5955 www.aham.org provides information on air cleaners on their AHAM-certified Clean Air Delivery Rate site at www.cadr.org AHAM conducts four certification programs for each category - room air cleaners, room air conditioners, dehumidifiers and refrigerator/freezers. The air cleaner certification program is known as AC-1.
Baabor, Marcos G., Pedro F. Vázquez, and José A. Soriano Sánchez. "Automated nucleotomy and nucleolysis with ozone." In Advances in Minimally Invasive Surgery and Therapy for Spine and Nerves, pp. 97-101. Springer Vienna, 2011.
Abstract: - research using ozone for medical treatment
Lumbar and radicular pain due to HNP has been described since 1934. It is thought that the pain is caused by compression and by other local chemical mediators that are present in the area of interaction between the root and the disc.
With the objective of treating patients suffering from this syndrome and with a percutaneous minimally invasive approach, we designed a mixed technique: percutaneous automated nucleotomy plus nucleolysis and periradicular infiltration with ozone.
A retrospective study of 105 patients was conducted, including 60 men and 45 women with an average age of 43 years. All patients were treated with that technique between November 2006 and August 2008. Clinical follow-up of 15.2 months was provided by telephone, utilizing a modified Mac Nab scale. The results were as follows: 60% excellent, 22.8% good (82.8% success), 9.6% acceptable, 7.6% poor. From the eight patients that reported poor results, five were considered to have recurrent symptoms (4.8%), because they had initially shown a period of significant improvement post operatively. Morbidity was manifested by transient pain and muscle spasms in the post operative area (2.8%).
We conclude that this new mixed technique, compared to automated percutaneous nucleotomy alone, may be more widely utilized by broadening the indications, with acceptable results.
(Blocks Hernia Nucleolysis Nucleotomy Nucleus pulposus Ozone Percutaneous Radicular pain)
California Department of Health Services, Indoor Air Quality Program, 850 Marina Bay Parkway, Suite G365/EHL, Richmond, CA 94804. DHS-IAQ Program Assistance Line: (510) 620-2874, Fax: (510) 620-2825
Castillejos, Margarita, Diane R. Gold, Andrew I. Damokosh, Paulina Serrano, George Allen, William F. McDonnell, Douglas Dockery, Silvia Ruiz Velasco, Mauricio Hernandez, and Carl Hayes. "Acute effects of ozone on the pulmonary function of exercising schoolchildren from Mexico City." American journal of respiratory and critical care medicine 152, no. 5 (1995): 1501-1507. Abstract:
The acute effects of ozone (O3) on the change in lung function before and after exercise was assessed in 22 boys and 18 girls from 7 1/2 to 11 yr of age tested up to eight times over a 1 1/2-yr period outdoors (under a tarpaulin) at a school in Mexico City. Ozone and particulates were monitored at an adjacent government station, in the school yard, and under the tarp. Subjects were selected to oversample children with chronic respiratory symptoms, although children with active asthma under regular medication or FEV1 < 80% predicted were excluded.
Of the participants, 21 had chronic cough, chronic phlegm, or ever wheeze with colds or apart from colds.
Children performed two cycles of treadmill exercise (15 min) and rest (15 min) for a total of 1 h of intermittent exercise. Most subjects attained the target minute ventilation of 35 L/min/m2. Subjects exercised alternately during low ozone hours (8:00-10:00 A.M.) and during peak O3 hours (12:00-2:00 P.M.), to assure a range of exposures.
On 85% of exercise days, the maximum daily 1-h average for ambient O3 exceeded the Mexican guideline of 110 parts per billion (ppb). O3 exposure during the hour of exercise was divided into quintiles, and the response was adjusted for repeated measures, subject having a cold, and prior outdoor exercise. Ambient O3 in the fifth quintile (mean = 229 ppb) was associated with a percentage change in FVC (-1.43% +/- 0.70), FEV1 (-2.85% +/- 0.79), FEF25-75% (-6.32 +/- 1.87) and FEV1 (-1.41% +/- 0.46). ...
Dorado-Martínez, Claudia, Cristina Paredes-carbajal, Dieter Mascher, Gabino Borgonio-Pérez, and Selva Rivas-arancibia. "Effects of different ozone doses on memory, motor activity and lipid peroxidation levels, in rats." International journal of neuroscience 108, no. 3-4 (2001): 149-161.
Abstract: Ozone is one of the main atmospheric pollutants. Its inhalation causes an increase in free radicals, when these free radicals are not compensated by antioxidants, it leads to an oxidative stress state. This oxidative stress state has been implicated in neurodegenerative processes. To determine the effects of oxidative stress caused by exposure to ozone on memory and motor activity, we used 120 male Wistar rats exposed to one of the following ozone doses, (0.0, 0.1, 0.4, 0.7, 1.1 and 1.5 ppm), for four hours. After ozone exposure, short and long term memory of a one trial passive avoidance test were measured, and motor activity was registered for five minutes, in 10 rats of each group. In 16 rats exposed to 0.0, 0.4, 0.7 or 1.1 ppm lipid peroxidation levels from frontal cortex, hippocampus, striatum and cerebellum, were measured.
Results show that ozone, causes memory impairment from doses of 0.7 ppm, decrease in motor activity from doses of 1.1 ppm, and increase in lipid peroxidation levels from doses of 0.4 ppm, that increase with the dose.
Golden, J. A., J. A. Nadel, and H. A. Boushey. "Bronchial Hyperirritability in Healthy Subjects after Exposure to Ozone 1, 2." American Review of Respiratory Disease 118, no. 2 (1978): 287-294. Abstract:
We studied the effect of a 2-hour exposure to 0.6 ppm of ozone on bronchial reactivity in 8 healthy, nonsmoking subjects by measuring the increase in airway resistance (Raw) produced by inhalation of histamine diphosphate aerosol (1.6 per cent, 10 breaths). Before exposure to ozone, histamine increased the mean Raw from 1.2 to 1.8 cm H2O per liter per sec.
Immediately after exposure to ozone, the mean baseline Raw was unchanged, but the mean response to histamine was significantly greater than the pre-ozone response (Raw = 3.3 cm H2O per liter per sec; P<0.05). For the group, this increase disappeared 1 day after exposure to ozone, although 2 subjects still had a significantly increased response to histamine for more than 1 week after exposure. In 4 subjects, pretreatment with atropine sulfate aerosol (0.1 to 0.2 mg per kg of body weight) blocked the increase in Raw produced by histamine after exposure to ozone.
We concluded that brief exposure to 0.6 ppm of ozone produces bronchial hyperirritability via cholinergic postganglionic pathways, probably by damaging airway epithelium and thereby sensitizing bronchial irritant receptors.
Gryparis, Alexandros, Bertil Forsberg, Klea Katsouyanni, Antonis Analitis, Giota Touloumi, Joel Schwartz, Evangelia Samoli et al. "Acute effects of ozone on mortality from the “air pollution and health: a European approach” project." American journal of respiratory and critical care medicine 170, no. 10 (2004): 1080-1087. Abstract:
the Air Pollution and Health: A European Approach (APHEA2) project, the effects of ambient ozone concentrations on mortality were investigated. Data were collected on daily ozone concentrations, the daily number of deaths, confounders, and potential effect modifiers from 23 cities/areas for at least 3 years since 1990. Effect estimates were obtained for each city with city-specific models and were combined using second-stage regression models.
No significant effects were observed during the cold half of the year.
For the warm season, an increase in the 1-hour ozone concentration by 10 μg/m3 was associated with a 0.33% (95% confidence interval [CI], 0.17–0.52) increase in the total daily number of deaths, 0.45% (95% CI, 0.22–0.69) in the number of cardiovascular deaths, and 1.13% (95% CI, 0.62–1.48) in the number of respiratory deaths. The corresponding figures for the 8-hour ozone were similar.
The associations with total mortality were independent of SO2 and particulate matter with aerodynamic diameter less than 10 μm (PM10) but were somewhat confounded by NO2 and CO. Individual city estimates were heterogeneous for total (a higher standardized mortality rate was associated with larger effects) and cardiovascular mortality (larger effects were observed in southern cities). The dose–response curve of ozone effects on total mortality during the summer did not deviate significantly from linearity.
Hazucha, Milan J., David V. Bates, and PHILIP A. Bromberg. "Mechanism of action of ozone on the human lung." Journal of Applied Physiology 67, no. 4 (1989): 1535-1541. Abstract:
Fourteen healthy normal volunteers were randomly exposed to air and 0.5 ppm of ozone (O3) in a controlled exposure chamber for a 2-h period during which 15 min of treadmill exercise sufficient to produce a ventilation of approximately 40 l/min was alternated with 15-min rest periods. Before testing an esophageal balloon was inserted, and lung volumes, flow rates, maximal inspiratory (at residual volume and functional residual capacity) and expiratory (at total lung capacity and functional residual capacity) mouth pressures, and pulmonary mechanics (static and dynamic compliance and airway resistance) were measured before and immediately after the exposure period. After the postexposure measurements had been completed, the subjects inhaled an aerosol of 20% lidocaine until response to citric acid aerosol inhalation was abolished. All of the measurements were immediately repeated.
We found that the O3 exposure
1) induced a significant mean decrement of 17.8% in vital capacity (this change was the result of a marked fall in inspiratory capacity without significant increase in residual volume),
2) significantly increased mean airway resistance and specific airway resistance but did not change dynamic or static pulmonary compliance or viscous or elastic work,
3) significantly reduced maximal transpulmonary pressure (by 19%) but produced no changes in inspiratory or expiratory maximal mouth pressures, and
4) significantly increased respiratory rate (in 5 subjects by more than 6 breaths/min) and decreased tidal volume.
Hoek, Gerard, Paul Fischer, Bert Brunekreef, Erik Lebret, Peter Hofschreuder, and Marcel G. Mennen. "Acute effects of ambient ozone on pulmonary function of children in the Netherlands." American review of respiratory disease 147 (1993): 111-111.
Jörres, R., Dennis Nowak, and Helgo Magnussen. "The effect of ozone exposure on allergen responsiveness in subjects with asthma or rhinitis." American journal of respiratory and critical care medicine 153, no. 1 (1996): 56-64. Abstract:
The aim of this study was to determine whether ozone enhances bronchial responsiveness to allergens in subjects with allergic asthma, or facilitates a bronchial response in subjects with allergic rhinitis. Twenty-four subjects with mild stable allergic asthma, 12 subjects with allergic rhinitis without asthma, and 10 healthy subjects participated in the study. Subjects breathed 250 ppb ozone or filtered air (FA) for 3 h of intermittent exercise. Airway responsiveness to methacholine was determined 1 h before and after exposures, and allergen responsiveness 3 h after exposures.
We determined the concentration of methacholine (PC20FEV1) and the dose of allergen (PD20FEV1) producing a 20% fall in FEV1. In the subjects with asthma, FEV1 decreased by 12.5 +/- 2.2% (mean +/- SEM; p = 0.0001), PC20FEV1 of methacholine by 0.91 +/- 0.19 doubling concentrations (p = 0.0001) and PD20FEV1 of allergen by 1.74 +/- 0.25 doubling doses (p < 0.0001) after ozone compared with FA.
The changes in lung function, methacholine, and allergen responsiveness did not correlate with each other.
In the subjects with rhinitis, mean FEV1 decreased by 7.8% and 1.3% when ozone or FA, respectively, were followed by allergen inhalation (p = 0.035).
Therefore, our data suggest that short-term exposure to ozone can increase bronchial allergen responsiveness in subjects with mild allergic asthma or rhinitis.
Linn, William S., Ramon D. Buckley, Charles E. Spier, Raymond L. Blessey, Michael P. Jones, D. Armin Fischer, and Jack D. Hackney. "Health Effects of Ozone Exposure in Asthmatics 1–3." American Review of Respiratory Disease 117, no. 5 (1978): 835-843.
Lippmann, Morton. "Health effects of ozone a critical review." Japca 39, no. 5 (1989): 672-695. Abstract:
Health and pollution control professionals and the general public need to develop a more complete understanding of the health effects of ozone (O3) because:
1) we have been unable to significantly reduce ambient O3 levels using current strategies and controls;
2) in areas occupied by more than half of the U.S. population, current peak ambient O3 concentrations are sufficient to elicit measurable transient changes in lung function, respiratory symptoms, and airway inflammation in healthy people engaged in normal outdoor exercise and recreational activities;
3) the effects of O3 on transient functional changes are sometimes greatly potentiated by the presence of other environmental variables; and
4) cumulative structural damage occurs in rats and monkeys exposed repetitively to O3 at levels within currently occurring ambient peaks, and initial evidence from dosimetry models and interspecies comparisons indicate that humans are likely to be more sensitive to O3 than rats. The extent and significance of these effects, and the multibillion dollar costs of ambient O3 controls need to be considered in any future revisions of ambient standards and the Clean Air Act.
The transient effects of O3 are more closely related to cumulative daily exposure than to one hour peak concentrations, and future revisions of the ambient standard for O3 should take this into account. The effects of long-term chronic exposure to O3 remain poorly defined, but recent epidemiologic and animal inhalation studies suggest that current ambient levels are sufficient to cause premature aging of the lungs. More research is needed to determine the need for a standard with a seasonal or annual average concentration limit.
McDonnell, William F., Donald H. Horstman, M. J. Hazucha, E. Seal, E. D. Haak, S. A. Salaam, and D. E. House. "Pulmonary effects of ozone exposure during exercise: dose-response characteristics." Journal of applied physiology 54, no. 5 (1983): 1345-1352. Abstract: Because minimal data are available regarding the pulmonary effects of ozone (O3) at levels less than 0.27 ppm, six groups of healthy young males were exposed for 2.5 h to one of the following O3 concentrations: 0.0, 0.12, 0.18, 0.24, 0.30, or 0.40 ppm. Fifteen-minute periods of rest and exercise (65 l/min minute ventilation) were alternated during the first 2 h of exposure. Coughing was observed at all levels of O3 exposure.
Small changes in forced-expiratory spirometric variables [forced vital capacity (FVC), forced expiratory volume in 1 s, and mean expiratory flow rate between 25 and 75% FVC] were observed at 0.12 and 0.18 ppm O3, and larger changes were found at O3 levels greater than or equal to 0.24 ppm. Changes in tidal volume and respiratory frequency during exercise, specific airway resistance, the presence of pain on deep inspiration, and shortness of breath occurred at O3 levels greater than or equal to 0.24 ppm.
In conclusion, pulmonary effects of O3 were observed at levels much lower than that for which these effects have been previously described. Stimulation of airway receptors is probably the mechanism responsible for the majority of observed changes; however, the existence of a second mechanism of action is postulated.
Menzel, Daniel B. "Ozone: an overview of its toxicity in man and animals." (1984): 181-204. Abstract:
Ozone is one of the most toxic and ubiquitous air pollutants. This review focuses on the toxic effects of ozone in animals and on the similarities and disimilarities between the toxic effects in animals and humans. The molecular basis for the toxicity of ozone is discussed, based on the vigorous oxidizing properties of ozone.
Despite the existence of anatomical differences between human, subhuman primate, and dog lungs versus common experimental rodent lungs, the anatomical lesion of ozone inhalation occurs at the functionally equivalent site of the junction between the conducting airway and the respiratory region. Ciliated cells of the upper airways and the type 1 cell of the centriacinar region are most affected. Type 2 cell proliferation is a hallmark of ozone toxicity. A wide variety of biochemical and physiological changes have been noted in several animal species and in humans.
Considerable evidence for a free‐radical‐mediated or lipid peroxide‐mediated toxicity is evident, especially in the induction of the glutathione peroxidase system and the protective effects of vitamins C and E. Ozone appears to be a weak mutagen and to produce chromosomal abnormalities.
Defects in defense against airborne infection are present in animals, which are more susceptible to airborne infection after ozone exposure.
Epidemiological studies, however, fail to detect increased respiratory infections in humans due to ozone.
Despite the variety of toxic effects, few qualitative differences between species are apparent; rather, quantitative differences do occur. Ozone may thus be an ideal compound for quantitative extrapolation of toxicity from animals to humans.
Preisser, Alexandra M., Lygia T. Budnik, and Xaver Baur. "Health effects due to fumigated freight containers and goods: how to detect, how to act." International maritime health 63, no. 3 (2012): 133-139. Abstract:
Headache, concentration and memory disorders, dizziness and nausea, skin irritation, respiratory distress, and muscle cramps — isolated or in various combinations — may be the result of acute or chronic intoxication by fumigants. The occurrence of these symptoms in workers who are engaged in the opening and unloading of containers, unpacking of imported goods, ventilating of containers, or working on bulk carriers are urgent indications of intoxication by fumigants or other toxic chemical residues in the transported goods.
The severity of the disorder depends on the concentration and duration of exposure, distribution and release of the fumigant, its kinetics, the individual susceptibility of the person, as well as any simultaneous exposure to other toxic substances. Physical symptoms, acute and chronic health effects due to contact with fumigants, are complex and difficult to discover.
In this article we explain how to identify the guiding symptoms and describe the appropriate diagnostic steps and the prevention of such events on cargo vessels as well as in the logistics and the handling of imported goods.
Reed, Dwayne, Sally Glaser, and John Kaldor. "Ozone toxicity symptoms among flight attendants." American journal of industrial medicine 1, no. 1 (1980): 43-54. Abstract:
Because of persistent complaints of ozone-toxicity type symptoms among crew members of commercial airlines, we undertook a survey to determine the extent of the problem and the associated flight factors. Self-reported questionnaires and flight diaries were completed by 1,330 flight attendants, (FAs) working for three different airlines.
Ozone-toxicity type symptoms were reported three or four times more frequently by FAs with airlines flying at high altitudes than by those with low-flying airlines.
When examined by characteristics of flights, the ozone-toxicity type symptoms were significantly associated with flight altitude, duration and type of aircraft, but not with years worked, sex, medical history, or home residence. Other symptoms indicative of fatigue or stress were mainly associated with flight duration.
While these indirect data cannot implicate ozone specifically, they offer evidence that ozone-related health problems do exist among a large proportion of FAs.
Scheel, Lester D., Olga J. Dobrogorski, John T. Mountain, Joseph L. Svirbely, and Herbert E. Stokinger. "Physiologic, biochemical, immunologic and pathologic changes following ozone exposure." Journal of applied physiology 14, no. 1 (1959): 67-80. Abstract: A detailed study of physiologic, biochemical, immunologic and pathologic changes resulting from acute and repeated acute injuries due to inhalation of ozone is reported. This study defines the primary chemical reaction of ozone with constituents of the body, the response of the body to the presence of the toxic substance, the physiologic functional alterations produced by acute and repeated acute injuries due to inhalation of this gas and the pathology produced by these injuries in rabbits, mice and rats.
The data presented show that ozone reacts with the proteins of lung tissue to produce a severe cellular irritation which alters cell wall permeability and leads to severe pulmonary edema.
Repeated acute injuries are shown to cause the development of fibrosis of the bronchioles and alveolar ducts, which limits the reserve capacity of the lung by causing the Hering-Breuer reflex to stop inspiration before complete inhalation can take place. Immunologic and biochemical changes observed which are characteristic of this type of injury are reported.
It has been shown that ozone reacts in a random fashion with proteins to produce a heterogeneous antigen which will stimulate an antibody response in rabbits.
The antigen created was shown to have characteristics similar to denatured protein.
The severe limitation of pulmonary function by reduced tidal volume and edema and the resulting pathologic changes are reported and discussed.
U.S. Chamber of Commerce, "Ozone National Ambient Air Quality Standards" [PDF] (August 2017) position statement, retrieved 2017/08/19, original source: https://www.uschamber.com/issue-brief/ozone-national-ambient-air-quality-standards
U.S. EPA- Indoor Air Quality Information Clearinghouse (IAQ INFO), PO Box 37133, Washington D.C. 20013-7133; by phone (800) 438-4318.
Weschler, Charles J. "Ozone's impact on public health: contributions from indoor exposures to ozone and products of ozone-initiated chemistry." Environmental health perspectives (2006): 1489-1496. See http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626413/ - Abstract:
Objective: The associations between ozone concentrations measured outdoors and both morbidity and mortality may be partially due to indoor exposures to ozone and ozone-initiated oxidation products. In this article I examine the contributions of such indoor exposures to overall ozone-related health effects by extensive review of the literature as well as further analyses of published data.
Findings Daily inhalation intakes of indoor ozone (micrograms per day) are estimated to be between 25 and 60% of total daily ozone intake. This is especially noteworthy in light of recent work indicating little, if any, threshold for ozone’s impact on mortality.
Additionally, the present study estimates that average daily indoor intakes of ozone oxidation products are roughly one-third to twice the indoor inhalation intake of ozone alone. Some of these oxidation products are known or suspected to adversely affect human health (e.g., formaldehyde, acrolein, hydroperoxides, fine and ultrafine particles). Indirect evidence supports connections between morbidity/mortality and exposures to indoor ozone and its oxidation products.
For example, cities with stronger associations between outdoor ozone and mortality tend to have residences that are older and less likely to have central air conditioning, which implies greater transport of ozone from outdoors to indoors.
Conclusions Indoor exposures to ozone and its oxidation products can be reduced by filtering ozone from ventilation air and limiting the indoor use of products and materials whose emissions react with ozone. Such steps might be especially valuable in schools, hospitals, and childcare centers in regions that routinely experience elevated outdoor ozone concentrations.
We do not completely share Weschler's conclusions because ozone itself is so highly volatile that ozone molecules don't tend to hang around long in buildings - unless an ozone generator is left turned on in the building itself. It would seem that a significant number of complaints about "ozone" may in fact be generated by odors emanating from oxicized materials that were exposed to an overdose of ozone during building "treatment" for odors. - OPNION - DF.
References for using ozone for drinking water disinfection
Arnold, Benjamin F., and John M. Colford Jr. "Treating water with chlorine at point-of-use to improve water quality and reduce child diarrhea in developing countries: a systematic review and meta-analysis." American journal of tropical medicine and hygiene 76, no. 2 (2007): 354-364.
Lazarova, V., Ph Savoye, M. L. Janex, E. R. Blatchley III, and M. Pommepuy. "Advanced wastewater disinfection technologies: state of the art and perspectives." Water Science and Technology 40, no. 4 (1999): 203-213.
Peeters, JOHAN E., E. Ares Mazas, Willy J. Masschelein, I. Villacorta Martiez de Maturana, and Emile Debacker. "Effect of disinfection of drinking water with ozone or chlorine dioxide on survival of Cryptosporidium parvum oocysts." Applied and environmental microbiology 55, no. 6 (1989): 1519-1522. Abstract: Demineralized water was seeded with controlled numbers of oocysts of Cryptosporidium parvum purified from fresh calf feces and subjected to different treatments with ozone or chlorine dioxide. The disinfectants were neutralized by sodium thiosulfate, and neonatal mice were inoculated intragastrically and sacrificed 7 days later for enumeration of oocyst production.
Preliminary trials indicated that a minimum infection level of 1,000 oocysts (0.1-ml inoculum) per mouse was necessary to induce 100% infection. Treatment of water containing 10(4) oocysts per ml with 1.11 mg of ozone per liter (concentration at time zero [C0]) for 6 min totally eliminated the infectivity of the oocysts for neonatal mice. A level of 2.27 mg of ozone per liter (C0) was necessary to inactivate water containing 5 x 10(5) oocysts per ml within 8 min. Also, 0.4 mg of chlorine dioxide per liter (C0) significantly reduced infectivity within 15 min of contact, although some oocysts remained viable.
Schoenen, D. "Role of disinfection in suppressing the spread of pathogens with drinking water: possibilities and limitations." Water research 36, no. 15 (2002): 3874-3888.
Shin, Gwy-Am, and Mark D. Sobsey. "Inactivation of norovirus by chlorine disinfection of water." Water research 42, no. 17 (2008): 4562-4568.
Sobsey, Mark D., Sanitation Water, and World Health Organization. "Managing water in the home: accelerated health gains from improved water supply/prepared by Mark D. Sobsey." (2002).
Xu, Xiaoming, Philip S. Stewart, and Xiao Chen. "Transport limitation of chlorine disinfection of Pseudomonas aeruginosa entrapped in alginate beads." Biotechnology and bioengineering 49, no. 1 (1996): 93-100.
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Kansas State University, department of plant pathology, extension plant pathology web page on wheat rust fungus: see http://www.oznet.ksu.edu/path-ext/factSheets/Wheat/Wheat%20Leaf%20Rust.asp
"A Brief Guide to Mold, Moisture, and Your Home",
U.S. Environmental Protection Agency US EPA - includes basic advice for building owners, occupants, and mold cleanup operations. See http://www.epa.gov/mold/moldguide.htm
US EPA - Mold Remediation in Schools and Commercial Building [Copy on file at /sickhouse/EPA_Mold_Remediation_in_Schools.pdf ] - US EPA
US EPA - Una Breva Guia a Moho - Hongo [Copy on file as /sickhouse/EPA_Moho_Guia_sp.pdf - en Espanol
Allergies, Allergens, Allergy Testing in Buildings - References & Products
"IgG Food Allergy Testing by ELISA/EIA, What do they really tell us?" Sheryl B. Miller, MT (ASCP), PhD, Clinical Laboratory Director, Bastyr University Natural Health Clinic - ELISA testing accuracy: Here is an example of Miller's critique of ELISA
http://www.betterhealthusa.com/public/282.cfm - Townsend Letter for Doctors and Patients
The critique included in that article raises compelling questions about IgG testing assays, which prompts our interest in actually screening for the presence of high levels of particles that could carry allergens - dog dander or cat dander in the case at hand.
http://www.tldp.com/issue/174/IgG%20Food%20Allergy.html contains similar criticism in another venue but interestingly by the same author, Sheryl Miller. Sheryl Miller, MT (ASCP), PhD, is an Immunologist and Associate Professor of Basic and Medical Sciences at Bastyr University in Bothell, Washington. She is also the Laboratory Director of the Bastyr Natural Health Clinic Laboratory.
Allergens: Testing for the level of exposure to animal allergens is discussed at http://www.animalhealthchannel.com/animalallergy/diagnosis.shtml (lab animal exposure study is interesting because it involves a higher exposure level in some cases
Allergens: WebMD discusses allergy tests for humans at webmd.com/allergies/allergy-tests
Associations: Sick House, Sick Building, SBS - Air Quality, Government, Private Associations and Information Resources
Atlas of Clinical Fungi, 2nd Ed., GS deHoog, J Guarro, J Gene, & MJ Figueras, Centraalbureau voor Schimmelcultures, Universitat Rovira I Virgili, 2000, ISBN 90-70351-43-9 (you can buy this book at Amazon) - The Atlas of Clinical Fungi is also available on CD ROM
Atlas of Indoor Mold, Online Clinical Mold Atlas, Toxins, Pathogens, Allergens and Other Indoor Particles - Medical Health Effects of Mold (separate online document)
"A Brief Guide to Mold, Moisture, and Your Home", U.S. Environmental Protection Agency US EPA - includes basic advice for building owners, occupants, and mold cleanup operations. See http://www.epa.gov/mold/moldguide.htm
"Disease Prevention in Home Vegetable Gardens,"
Department of Plant Microbiology and Pathology,
Department of Horticulture, University of Missouri Extension - extension.missouri.edu/publications/DisplayPub.aspx?P=G6202
Fifth Kingdom, Bryce Kendrick, ISBN13: 9781585100224, is available from the InspectAPedia online bookstore - we recommend the CD-ROM version of this book. This 3rd/edition is a compact but comprehensive encyclopedia of all things mycological. Every aspect of the fungi, from aflatoxin to zppspores, with an accessible blend of verve and wit. The 24 chapters are filled with up-to-date information of classification, yeast, lichens, spore dispersal, allergies, ecology, genetics, plant pathology, predatory fungi, biological control, mutualistic symbioses with animals and plants, fungi as food, food spoilage and mycotoxins.
Rodents, Mice, Squirrel Control - I find high levels of mouse and rodent dander, fecal dust, and urine-contaminated dust in some buildings,
and high levels of these materials in building insulation in those locations. If you have a mouse problem, particularly if mice and their waste (fecals or urine) are contaminating
the building HVAC or building insulation, may need both steps to clean up or remove infected materials and steps to stop an ongoing
rodent problem. If squirrels are a problem, the cleanup needs to include closing off entry openings into the building. Get some
help from a licensed pest control expert.
Carson, Dunlop & Associates Ltd., 120 Carlton Street Suite 407, Toronto ON M5A 4K2. Tel: (416) 964-9415 1-800-268-7070 Email: firstname.lastname@example.org. The firm provides professional home inspection services & home inspection education & publications. Alan Carson is a past president of ASHI, the American Society of Home Inspectors. Thanks to Alan Carson and Bob Dunlop, for permission for InspectAPedia to use text excerpts from The Home Reference Book & illustrations from The Illustrated Home. Carson Dunlop Associates' provides extensive home inspection education and report writing material.
The Illustrated Home illustrates construction details and building components, a reference for owners & inspectors. Special Offer: For a 5% discount on any number of copies of the Illustrated Home purchased as a single order Enter INSPECTAILL in the order payment page "Promo/Redemption" space.
TECHNICAL REFERENCE GUIDE to manufacturer's model and serial number information for heating and cooling equipment, useful for determining the age of heating boilers, furnaces, water heaters is provided by Carson Dunlop, Associates, Toronto - Carson Dunlop Weldon & Associates Special Offer: Carson Dunlop Associates offers InspectAPedia readers in the U.S.A. a 5% discount on any number of copies of the Technical Reference Guide purchased as a single order. Just enter INSPECTATRG in the order payment page "Promo/Redemption" space.
The Home Reference Book - the Encyclopedia of Homes, Carson Dunlop & Associates, Toronto, Ontario, 25th Ed., 2012, is a bound volume of more than 450 illustrated pages that assist home inspectors and home owners in the inspection and detection of problems on buildings. The text is intended as a reference guide to help building owners operate and maintain their home effectively. Field inspection worksheets are included at the back of the volume.
Special Offer: For a 10% discount on any number of copies of the Home Reference Book purchased as a single order. Enter INSPECTAHRB in the order payment page "Promo/Redemption" space. InspectAPedia.com editor Daniel Friedman is a contributing author.
Special Offer: Carson Dunlop Associates offers InspectAPedia readers in the U.S.A. a 5% discount on these courses: Enter INSPECTAHITP in the order payment page "Promo/Redemption" space. InspectAPedia.com editor Daniel Friedman is a contributing author.
The Horizon Software System manages business operations,scheduling, & inspection report writing using Carson Dunlop's knowledge base & color images. The Horizon system runs on always-available cloud-based software for office computers, laptops, tablets, iPad, Android, & other smartphones