East Valley Inspections
480-747-7108
BLOG.EASTVALLEYINSPECTIONS.COM

"East Valley Inspections" is ranked in the Top 3 among home inspectors in Phoenix.

Home Inspection Services, Phoenix, AZ Summer is on us and your AC units will be running non-stop so make sure to check your condensate drains. Make sure that they are not plugged and water can flow through freely.
Posted by East Valley Inspections at 6/8/2011 7:23 AM | Add Comment

Is Hidden Mold at Home Making You Sick?

Check out the link below,
http://abcnews.go.com/WNT/story?id=131638&page=1

Make sure you check your home often for mold and if you are not sure call us out to test. It is quick and easy.
Posted by East Valley Inspections at 6/7/2011 10:10 AM | Add Comment

Seasonal Pollen

The Environmental Reporter
August 2010Volume 8 | Issue 8

Seasonal Pollen
By Shamika Edwards, EMLab P&K Analyst and NAB Certified Pollen & Mold Spore Counter

Each spring, summer, and fall, the season is filled with lush colors of blooming trees, grasses, and weeds, which release tiny particles. The tiny particles are known as pollen. Pollen has several vectors it uses for mobility; anemophily (movement via wind), entomophily (movement via insects), ornithophily (movement via birds), hydrophily (movement via water), chiropterophily (movement via bats), and zoophily (movement via other animals). The pollen grains proceed by hitching a ride on the currents of the air. Then, nature does its part to generate variation and speciation through cleistogamy (self-pollination), and allogamy (cross-pollination). Although the main purpose of pollen is to fertilize other plants, many times it never succeeds in making it to its intended target. Instead, pollen enters human noses and throats, triggering a type of seasonal allergic rhinitis typically called pollen allergy or hay fever.

Trees, grasses and weeds have a very distinct period of pollination that typically do not vary from year to year. Generally, the entire pollen season lasts from February through October with pine having an elevated pollen production throughout. Even though it is abundant, pine pollen is seldom an important allergen. The pollinating season, however, starts later in the spring the further north one goes. In warmer places, pollination can occur year-round. In most southern states, tree-pollinating season commences in late December and ends in May. In the South Texas region, a unique fall pollination of Ulmus (elm) and evergreens such as Juniperus (junipers). Also in Texas, mountain cedar pollen (Juniperus ashei) is another unique pollination period that occurs in December and January. Typically, grass pollen begins in late May followed by the weed season in June and July. Starting in August, weed pollen increases in the environment and by the end of August, ragweed pollen begins to dominate the air.

Microscopic photo of Pine Tree Pollen

Figure 1: Microscopic photo of Pine (Family: Pinaceae; Genus: Pinus) pollen showing characteristic air bladders giving it the appearance of Mickey Mouse ears.
Copyright © 2010 EMLab P&K		 Microscopic Photo of Elm Tree Pollen

Figure 2: Microscopic photo of Elm (Family: Ulmaceae; Genus: Ulmus) pollen produced from January through April.
Copyright © 2010 EMLab P&K

Seasonal allergic rhinitis is often caused by tree pollen in the early spring. The chemical makeup of pollen is the basic factor that determines whether the pollen is likely to cause any type of allergic symptom. During the late spring and early summer, grasses often cause symptoms. Hay fever is caused by weeds in the late summer and early fall. In the late fall, unique to Central Texas, is a seasonal allergic rhinitis known as cedar fever. Trees that produce allergenic pollen include oak, ash, elm, hickory, pecan, box elder, and mountain cedar. Among North American plants, weeds are the most prolific producers of allergenic pollen. Usually ragweed is the major culprit, but others of importance are sagebrush, redroot pigweed, lamb's quarters, Russian thistle (tumbleweed), and English plantain. Grasses are known to be a significant source of allergenic pollen. Timothy grass, Kentucky bluegrass, johnsongrass, Bermuda grass, redtop grass, orchard grass, and sweet vernal grass are all known to produce highly allergenic pollen.

Microscopic photo of Juniper Tree Pollen

Figure 3: Microscopic photo of Juniper (Family: Cupressaceae; Genus: Juniperus) pollen.
Copyright © 2010 EMLab P&K		 Microscopic photo of Grass Pollen

Figure 4: Microscopic photo of Grass (Family: Poaceae) pollen produced May through October.
Copyright © 2010 EMLab P&K

A pollen count, which is familiar to many people from local weather reports, is a measure of how much pollen is in the air. This count represents the concentration of all the pollen, expressed as grains of pollen per cubic meter of air collected over 24 hours. This count is generated by certified Pollen Counters of the National Allergy Bureau (NA. There are only 106 certified pollen counters in the country and 81 NAB-certified counting stations across the United States, Canada and Argentina. Each count comes from a NAB counting station, which is part of the American Academy of Allergy, Asthma and Immunology's (AAAAI) Aeroallergen Network, responsible for reporting current pollen and mold spore levels to the public.

Microscopic photo of Ash Tree Pollen

Figure 5: Microscopic photo of Ash (Family: Oleaceae; Genus: Fraxinus) pollen produced from March through June.
Copyright © 2010 EMLab P&K		 Microscopic photo of Ragweed Weed Pollen

Figure 6: Microscopic photo of Ragweed (Family: Asteracea; Genus: Ambrosia) pollen produced from August through October.
Copyright © 2010 EMLab P&K

Weather has significant effects on pollen release. The most pollen will be released on warm, dry, sunny, and windy days. Cold temperatures and high humidity delay pollen release, and precipitation washes pollen out of the air. Certain weather conditions can increase or decrease the amount of pollination. If the winter is mild, then typically the allergy season will begin early because the trees will release their pollen earlier than normal. If, on the other hand, a mild spring occurs this will intensify the tree pollen release for the spring. Winds are another contributing factor, which can spread the pollen rapidly, thus increasing the pollination. The windier the conditions are, the higher distribution of pollen within the air. If the weather generates a late freeze, then tree pollination will be delayed or could possibly decrease. Increased rain amounts in fall or winter can cause an increase in spring tree pollination amounts. Increased rain amounts in spring can stimulate grass growth, thus producing more grass pollen. The lifeline of pollen depends on the weather, through dry days, breezy days, rainy days, foggy days and, humid days.

References:
1. Farrar JL, Trees of the Northern United States and Canada. Ames, IA: Iowa State University Press; 1995.

2. Smith, E. Grant, Sampling and Identifying Allergenic Pollen and Molds. TX: Blewstone Press; 2000.

3. Sharma Smrity. Allergy season at its worst in years in US. The Money Times. April 16, 2010.


The data and other information contained in this newsletter are provided for informational purposes only and should not be relied upon for any other purpose. EMLab P&K hereby disclaims any liability for any and all direct, indirect, punitive, incidental, special or consequential damages arising out of the use or interpretation of the data or other information contained in, or any actions taken or omitted in reliance upon, this newsletter. Images included in this newsletter are property of EMLab P&K, unless otherwise specified.

EMLab P&K: When quality and accuracy are critical.
Posted by East Valley Inspections at 4/21/2011 3:33 PM | Add Comment

Monthly Environmental

The Environmental Reporter
 Volume 9 | Issue 2

Hello Geoff,

I hope you're doing well and enjoying spring. I also hope that you'll find the following article about the insects, allergy and indoor air quality by Dr. Joseph Manfrida both interesting and useful.

With best wishes,
Dave Gallup



Insects, Allergy and Indoor Air Quality
By Joseph P. Manfrida, Ph.D., EMLab P&K Technical Trainer and Lean Six Sigma Manager

With estimates that the average person spends approximately 23 hours every day indoors or in enclosed environments, it's safe to make the assertion that indoor air quality is likely to have a dramatic effect on an individual's overall health1. Insects that make their way into our homes are believed to play a significant role in indoor air quality. Research has demonstrated that a variety of insects, including cockroaches, dust mites, ants, sheep blow flies and weevils are strongly linked to asthma and allergic reactions in the upper respiratory tract 2, 3, 4, 5, 6. Studies of roach penetration into homes in the United States indicate that the majority of homes (63%) have detectable levels of cockroach antigens. Of these homes, 10% have concentrations of cockroach antigen associated with increased upper respiratory health problems7. Unfortunately, the current state of research on the effect of insect particulates on human health is not as extensive as that on other types of indoor air contaminants. The mechanisms by which insects impact human health are not fully understood at this time. As a result, much of what we know is tentative and investigations into this area occasionally yield conflicting results. However, an examination of what we do know will help us to understand, and counter to the best of our ability, this potential threat to the well being of everyone who spends most of their days living and working indoors.

The effects of insects on human health in relation to indoor air quality can be characterized as an allergic response. An allergic response occurs when an individual is exposed to a particle (in this case we are concerned with a particle from an insect) to which their immune system reacts. These particles that can induce an immune system reaction are called antigens. Exposure to antigens cause immune cells (eosinophils) in an individual's body to release chemicals into the exposed person's bloodstream that cause the symptoms typical of an allergic reaction, including inflammation, swelling, watery eyes and nasal discharge8. The process by which the cells of an individual's immune system learn to recognize and react to antigens (thereby causing inflammation) is called sensitization. Though the biological mechanism of sensitization is not thoroughly understood at this time, in the generally accepted hypothesis of immune system function sensitization to a given antigen is more likely with increased exposure. Increased exposure can result from either being exposed to a greater amount of antigen, or from exposure to a smaller amount of antigen for a longer amount of time. Inflammation and allergic symptoms do not necessarily limit themselves to the site of exposure to the antigen. When inflammation occurs at a site in a person's body, other than where they come into contact with the antigen, it is referred to as being atopic. People who have atopic symptoms are more likely to develop asthma 9. Asthma is a particular form of atopic allergic reaction centered in the lungs and trachea that can lead to difficulty breathing. This form of atopic asthma can have a genetic precursor, though studies have shown that a genetic predisposition to atopic asthma is not always necessary for the symptoms to arise10. Furthermore, studies have demonstrated that individuals who have exhibited symptoms of atopic allergic reactions, such as asthma, are more readily sensitized to novel antigens than individuals who do not possess atopic symptoms11.

The previously discussed discoveries have lead researchers into a quandary while trying to puzzle out the root cause of asthma and its relationship to sensitization. How can asthma have a genetic component in some cases, but not in others? Why should having asthma predispose a person to rapid sensitization to novel antigens? Jonathan M. Gaffin, MD and Wanda Phipatanakul, MD, MS seek to answer the above questions and describe a mechanism for how asthma develops in their manuscript, The Role of Indoor Allergens in the Development of Asthma12. Summarized briefly, the proposed mechanism is that individuals exposed to a particular antigen for a protracted time will become sensitized and develop inflammation. The length of time required for this to occur is regulated both by genetic predisposition and the amount of antigen in the exposure. Individuals genetically predisposed to asthma progress faster than individuals who are not. Increased immune system activity, along with changes in the tissues lining the trachea and lungs of asthmatic individuals, allow them to become sensitized more rapidly after exposure to new antigens. If this process is left unchecked, chronic asthma can alter the lining of the trachea and lungs to the extent that the individual becomes inclined to suffer from the extreme form of allergic reaction known as anaphylaxis, a condition that can be fatal13. While further research into the pathophysiology of asthma will be necessary to confirm the mechanism outlined by Gaffin and Phipatanakul, if their ideas are correct, then early intervention in the process could prevent the development of asthma or mitigate the worst of its symptoms.

As mentioned earlier, insects have been known to produce antigens that cause allergic reactions. Of all the insects studied, two of the most common have been the German cockroach (Blattella germanica) and the house dust mite (various Dermatophagoidesspecies), due to their ubiquity in human communities. Cockroaches produce fifteen to twenty different proteins that are currently believed to be antigenic in humans, but two antigens in particular, Bla g1 and Bla g2, are most commonly associated with human health effects14, 15. Exposure to cockroach antigens is common in the human population. In the United States, it is currently estimated that 26.1% of the population has been exposed to these antigens in concentrations significant enough to cause sensitization16.

Dust mite antigens include the commonly studied antigens Der p1 and Der f1 in addition to at least twelve other known antigens17. Evidence is accumulating that dust mite antigens are particularly insidious for two reasons. First, dust mite allergy is inclined to be perennial and less seasonal than other insect allergies18. Dust mites thrive in the sleeping quarters of our homes, and are generally not affected by seasonal temperature change to the same degree as larger insects that have to live in spaces with less climate control. Since they are not exposed to dramatic temperature changes, dust mite populations (and the amount of antigen they produce) remain largely constant throughout the year. Second, dust mite antigens appear to be correlated with human health effects outside of allergic response. Children living in homes with concentrations of Der p1 of 2µg/g or greater, had more severe asthma symptoms than those who did not, even though these children did not exhibit sensitization to dust mite antigen when they were tested, indicating that the effects were not likely to have been due to an immune-response mediated reaction to dust mites19. Additional testing in children with asthma (who had experienced allergic sensitization) and children without asthma (those who had not been sensitized) who were exposed to mite antigen concentrations of 4µg/g, showed that both groups experienced symptoms of bronchial hyperresponsiveness when given histamine, an asthma-like symptom20. If the asthma-like symptom were mediated by an allergic response to dust mite antigen, it would be expected that only the asthmatic children who had experienced allergic sensitization to dust mite antigen should have been affected. In both studies, the children examined showed no evidence of having been exposed to antigens from sources other than dust mites. This evidence points to a correlation between the presence of dust mite antigen and human health effects that are not an allergic response. At this time there is no known mechanism for how this occurs, but research to find a causal connection between these health effects and the presence of dust mite antigens is ongoing.

The effects of these antigenic particles from insects are exacerbated by their persistence. Since these antigens are of biological origin, it would be understandable if one were to postulate that their effects would be constrained by time. In many cases, biological materials lose their ability to trigger an immune reaction as the decay process deforms and breaks them down. Unfortunately, insect antigens have proven to be effective for long periods of time after having been shed. Researchers have demonstrated that cockroach antigens can remain present and capable of inducing an immune reaction in a given location for five years after cockroach removal21. This remarkable resistance to natural decay means that any attempt to control insect antigens in a given building must address both removal of the antigens as well as removal of the insects that generate them.

The process of detecting and remediating an insect contamination problem has been referred to in the scientific literature as Integrated Pest Management (IPM)22. IPM is a process that begins with an investigation of the extent of the problem, moves on to put initial remediation efforts in place, and then establishes a set of practices by the residents of the affected area to prevent the return of insect infestation and the contamination they can potentially bring. Initial investigation by most workers in the field of insect contamination will include an interview with the residents of a given facility, as well as a physical inspection of the area in question23. In residences, physical inspection typically focuses on kitchens, bathrooms, and bedrooms. Cockroaches tend to congregate in the kitchens and bathrooms of homes where water is readily available, while dust mites tend to be found in bedrooms where their primary food source (dead human skin cells) tends to accumulate in pillows, sheets and blankets23. Large scale physical inspection should include looking for signs of cracks or holes in the walls and foundation of a building which could admit cockroaches from the outside environment, in addition to an evaluation of housekeeping measures to suppress the availability of water and food resources that attract insects. Sampling for insect antigens can be performed to quantify the level of insect contamination in a building. Insect antigens tend to remain airborne for only a short period of time after disturbance; therefore it is most effective to collect dust samples for analysis24, 25. The concentration of antigens in the dust can be determined using an immunological assay known as the ELISA test. This test yields results in terms of the number of micrograms of antigen present per gram of dust. While the relevant research has not yet determined a specific concentration at which pathogenic effects will be developed in humans, it is generally accepted that concentrations of 2µg/g are sufficient to trigger sensitization in humans26. This concentration is therefore commonly an agreed on threshold for implementing extensive remediation efforts. Remediation efforts should include active extermination protocols to eliminate current insect infestation as well as the repair of any cracks or holes in the structure. Additionally, extensive cleaning efforts should be made and maintained to prevent the accumulation of food and water that will attract insects. Post-remediation dust sampling is used to confirm and quantify the success of remediation. Combined, these efforts have been demonstrated to reduce the concentration of insect antigens in contaminated buildings by 51%27. It should be noted that vigilance and continued effort is necessary to prevent subsequent recontamination. In the absence of extensive cleaning efforts on the part of residents in a decontaminated building, cockroach re-infestation has been demonstrated to occur in less than twelve months28.

There is currently no direct evidence indicating that remediation of cockroach infestation will help to relieve the symptoms of individuals already suffering from asthma29. Presumably, individuals who already have asthma will suffer reactions induced by antigens other than those that come from insects after the insect contamination has been removed. However, if the mechanism of asthma development outlined by Gaffin and Phipatanakul12 is correct, then it should be expected that the removal of insect antigens from a contaminated building will likely reduce the probability that individuals will develop asthma in the first place. This hopeful hypothesis is currently the subject of extensive scientific inquiry. Confirmation of this hypothesis could yield protocols for the reduction of asthma in the population by means of the maintenance of a properly clean indoor environment.

EMLab P&K offers dust analysis for antigens. In addition to the detection of the insect antigens Der p1, Der f1 and Bla g1, we also have the capability to measure the concentrations of dog antigen (Can f1), cat antigen (Fel d1), mouse antigen (Mus m1) and rat antigen (Rat n1). Contact us with any questions regarding antigenic contamination of indoor environments. Our technical experts are available to assist you.

References:
1. Gammage, Richard B., and Barry A. Berven. Indoor Air and Human Health, Second Edition. Boca Raton: Lewis Publishers, 1996. p. 200.

2. Cohn, Richard D., Samuel J. Arbes Jr., Renee Jaramillo, Laura H. Reid, and Darryl C. Zeldin. National prevalence and exposure risk for cockroach allergen in U.S. households. Environmental Health Perspectives 114.4 (April 2006): 522-526.

3. Spengler, John D., Jonathan M. Samet, and John F. McCarthy. Indoor Air Quality Handbook. New York: McGraw-Hill, 2001. p. 43.4-43.6.

4. Kaufman, G. L., B. H. Gandevia, T. E. Bellas, E. R. Tovey and B. A. Baldo. Occupational allergy in an entomological research centre. Clinical aspects of reactions to the sheep blowfly Lucilia cuprina. British Journal of Industrial Medicine 46 (1989): 473-478.

5. Kim, Cheol-Woo, Deok-In Kim, Soo-Young Choi, Jung-Won Park, and Chein-Soo Hong. Pharaoh ant (Monomorium pharaonis): newly identified important inhalant allergens in bronchial asthma. Journal of Korean Medical Science 20 (2005): 390-396.

6. Frankland, A. W., and J. A. Lunn. Asthma caused by the grain weevil. British Journal of Industrial Medicine 22 (1965): 157-159.

7. Cohn, Richard D., Samuel J. Arbes Jr., Renee Jaramillo, Laura H. Reid, and Darryl c. Zeldin. National prevalence and exposure risk for cockroach allergen in U.S. households. Environmental Health Perspectives 114.4 (April 2006): 522-526.

8. Yong, Tai-Soon, and Kyoung Yong Jeong. Household arthropod allergens in Korea. Korean Journal of Parasitology 47(October 2009): S143-S153.

9. Gent, Janneane F., Kathleen Belanger, Elizabeth W. Triche, Michael B. Bracken, William S. Beckett, and Brian P. Leaderer. Association of pediatric asthma severity with exposure to common household dust allergens. Environmental Research 109.6 (August 2009): 768-774.

10. King, Talmadge E. A New Look at the Pathophysiology of Asthma. Journal of the National Medical Association 91.8 (1999): 9S-15S.

11. Kim, Cheol-Woo, Deok-In Kim, Soo-Young Choi, Jung-Won Park, and Chein-Soo Hong. Pharaoh ant (Monomorium pharaonis): newly identified important inhalant allergens in bronchial asthma. Journal of Korean Medical Science 20 (2005): 390-396.

12. Gaffin, Jonathan M. and Wanda Phipatanakul. The role of indoor allergens in the development of asthma. Current Opinion in Allergy and Clinical Immunology 9.2 (April 2009): 128-135.

13. Kumar, Arvind, Suzanne S. Teuber and M. Eric Gershwin. Why do people die of anaphylaxis? - a clinical review. Clinical & Developmental Immunology 12.4 (December 2005): 281-287.

14. Potera, Carol. Working the bugs out of asthma. Environmental Health Perspectives 105.11 (November 1997): 1192-1194.

15. Yong, Tai-Soon, and Kyoung Yong Jeong. Household arthropod allergens in Korea. Korean Journal of Parasitology 47(October 2009): S143-S153.

16. Cohn, Richard D., Samuel J. Arbes Jr., Renee Jaramillo, Laura H. Reid, and Darryl c. Zeldin. National prevalence and exposure risk for cockroach allergen in U.S. Households. Environmental Health Perspectives 114.4 (April 2006): 522-526.

17. Spengler, John D., Jonathan M. Samet, and John F. McCarthy. Indoor Air Quality Handbook. New York: McGraw-Hill, 2001. p. 43.4-43.6.

18. Yong, Tai-Soon, and Kyoung Yong Jeong. Household arthropod allergens in Korea. Korean Journal of Parasitology 47(October 2009): S143-S153.

19. Gent, Janneane F., Kathleen Belanger, Elizabeth W. Triche, Michael B. Bracken, William S. Beckett, and Brian P. Leaderer. Association of pediatric asthma severity with exposure to common household dust allergens. Environmental Research 109.6 (August 2009): 768-774.

20. Sporik, Richard, Susan P. Squillace, Jim Mark Ingram, Gary Rakes, Richard W. Honsinger and Thomas A. E. Platts-Mills. Mite, cat and cockroach exposure, allergen sensitization, and asthma in children: a case-control study of three schools. Thorax 54 (1999): 675-680.

21. Potera, Carol. Working the bugs out of asthma. Environmental Health Perspectives 105.11 (November 1997): 1192-1194.

22. Sheehan, William J., Pitud A. Rangsithiechai, Rober A. Wood, Don Rivard, Sasawan Chinratanapisit, Matthew S. Perzanowski, Ginger L. Chew, James M. Seltzer, Elizabeth C. Matsui, and Wanda Phipatanakul. Pest and allergen exposure and abatement in inner - city asthma: a work group report of the American Academy of Allergy, Asthma & Immunology indoor allergy / air pollution committee. Journal of Clinical Immunology 125.3 (March 2010): 575-581.

23. O'Connor, George T. and Diane R. Gold. Cockroach allergy and asthma in a 30-year-old man. Environmental Health Perspectives 107.3 (March 1999): 243-247.

24. Yong, Tai-Soon, and Kyoung Yong Jeong. Household arthropod allergens in Korea. Korean Journal of Parasitology 47(October 2009): S143-S153.

25. Spengler, John D., Jonathan M. Samet, and John F. McCarthy. Indoor Air Quality Handbook. New York: McGraw-Hill, 2001. p. 43.4-43.6.

26. Dillon, H. Kenneth, ed., Ling-Ling Hung, and J. David Miller. Field Guide for the Determination of Biological Contaminants in Environmental Samples. American Industrial Hygiene Association Biosafety Committee, Virginia, 1996. p. 1-284.

27. Sheehan, William J., Pitud A. Rangsithiechai, Rober A. Wood, Don Rivard, Sasawan Chinratanapisit, Matthew S. Perzanowski, Ginger L. Chew, James M. Seltzer, Elizabeth C. Matsui, and Wanda Phipatanakul. Pest and allergen exposure and abatement in inner-city asthma: a work group report of the American Academy of Allergy, Asthma & Immunology indoor allergy / air pollution committee. Journal of Clinical Immunology 125.3 (March 2010) 575-581.

28. Ibid., Journal of Clinical Immunology, p560.

29. Gotzche, Peter G., Cecilia Hammarquist and Michael Burr. House dust mite control measures in the management of asthma: meta-analysis. British Medical Journal 317 (October 1998): 1105-1110.


The data and other information contained in this newsletter are provided for informational purposes only and should not be relied upon for any other purpose. EMLab P&K hereby disclaims any liability for any and all direct, indirect, punitive, incidental, special or consequential damages arising out of the use or interpretation of the data or other information contained in, or any actions taken or omitted in reliance upon, this newsletter. Images included in this newsletter are property of EMLab P&K, unless otherwise specified.

EMLab P&K: When quality and accuracy are critical.
Posted by East Valley Inspections at 4/1/2011 3:00 PM | View Comments (1) | Add Comment

Things you oughta know

10 Mold Facts for Homeowners, Landlords, Tenants, & Employers

  1. Airborne mold spores are everywhere both indoors and outdoors. Resident and employee health is at serious risk if there are elevated levels of mold spores indoors, as compared to an outdoor mold control test.
  2. The most dangerous indoor molds are Alternaria, Aspergillus, Chaetomium, Cladosporium, Fusarium, Mucor, Penicillium, and Stachybotrys. Mold testing and mold laboratory analysis are required to identify specific mold species.
  3. Molds spores can cause serious health problems even if the spores are dead or dormant (inactive while waiting for more moisture to resume growth). Even the smell of dead or dormant mold can make some mold-sensitive persons ill.
  4. It is impossible to get rid of all mold spores indoors. Some mold spores will always be present in house dust and floating in the air.
  5. The mold spores will not grow into mold colonies if there is insufficient moisture.  Indoor mold growth can and should be prevented or controlled by controlling moisture indoors. If organic materials are wet for more than 24 hours, mold growth can begin.
  6. Mold grows by eating and destroying organic building materials and other cellulose-based materials such as carpeting, upholstery, and clothing. The longer that mold grows, the more mold damage to the building.
  7. Cellulose is the main substance in the cell walls of plants (and thus of wood), and it is used in the manufacture of many organic building materials such as drywall, plasterboard, plywood substitutes, and ceiling tiles.
  8. Mold can grow hidden and undetected inside wall and ceiling cavities; beneath wallpaper, paneling, and carpeting; and inside heating and cooling equipment and ducts, attics, crawl spaces, and basements.
  9. Mold growth is often the result of a structural or construction defect, or of maintenance neglect, that allows moisture to enter the building.
  10. The owner or employer must first fix the water problem (roof leak, plumbing leak, high indoor humidity) that enables the mold to grow. Effective mold remediation requires killing the mold with an EPA-registered fungicide, removing it, and treating the cleaned area with an EPA-registered preventive fungicidal coating.

What Causes Indoor Mold Growth?

Mold can grow on virtually any organic substance or building material comprised of wood, wallpaper, drywall, carpet, paint, adhesives, fabrics, ducting and insulation. Mold is in the air everywhere and when it lands on a damp indoor spot with little or no UV light, it begins digesting and growing. This produces thousands of microscopic spores that are released into the air while the destructive organism eventually damages the materials on which they feed and grow.

Close-up of mold on a restoration project.Mold

Mold infestation and rampant growth usually occurs whenever water damage or other moisture problems in indoor environments go unaddressed or are treated improperly. Typical problem situations encountered are:

  • Natural weather disasters
  • Equipment malfunctions in a building
  • Poor facility design or maintenance
  • Improper cleanup after a problem
  • Delayed remediation after an event
 Mold growth behind floor trim.

Visible mold is typically only the tip of the iceberg, and usually a sign that the problem may already be extensive. It is not uncommon to find 10 times or more mold growth out of sight inside the crevices of a wall or within an HVAC system.

Posted by East Valley Inspections at 1/30/2009 3:54 AM | View Comments (7) | Add Comment
Serving the entire Phoenix/metro area. Copyright 2009. All rights reserved.
Blog Software