Pediatric Annals

ENVIRONMENTAL CHALLENGES FOR THE PEDIATRICIAN 

The "Fatal Four" Indoor Air Pollutants

Ruth A Etzel, MD, PHD

Abstract

A tremendous amount has been learned about the effects of the environment on human health since World War II. We now have a far better understanding that exposures once thought to be innocuous, such as to cigarette smoke, mercury, and molds, may actually pose threats to children's health. However, we have a long way to go toward integrating this knowledge into clinical practice. One major reason why we have not managed to integrate environmental health into practice is that we know little about the specific environments our patients call home.

Before World War II, more than half of the patients who saw a physician saw him in their home. This allowed the physician to identify possible environmental risks and to provide appropriate advice about preventing disease. When the physician entered the patient's home, he would note characteristics such as the growth of mold on ceilings and walls and the presence of insects and rodents. If the physician's nose detected tobacco's familiar odor, he could counsel the smoker about the importance of quitting.

Because we no longer visit the patient's home, we usually have little understanding of the environment in which the family lives. There is a sort of paradox here: we now know far more about the effects of environmental factors on human health, but we know far less about the specific environments in which our patients live. One time-saving way to integrate environmental health into practice is to provide families with a short "home inventory" questionnaire to complete at the first office visit1,2 (Table 1).

Another substantial change in the past three decades is that levels of outdoor air pollution have fallen dramatically, whereas levels of indoor air pollution have risen. The levels of indoor air pollutants are higher because, after the energy crisis of the 1970s, Americans began building more airtight homes, increased their use of indoor space heaters, and opened fewer windows for ventilation. Four indoor air pollutants^ - carbon monoxide, environmental tobacco smoke, toxigenic molds, and mercury vapor - are among the most important to discuss with parents because they may lead to serious illness or death in some children. Each is addressed in this article, and advice is offered for anticipatory guidance. For more information, the reader is referred to the American Academy of Pediatrics Handbook of Pediatric Environmental Health, which contains guidance on these four indoor air pollutants and other environmental hazards for children.2

Table

MERCURY VAPOR

Mercury vapor can be a fatal indoor air pollutant. Elemental mercury (quicksilver) is used in sphygmomanometers, thermometers, and thermostat switches. Dental amalgams contain approximately 50% mercury, as well as silver and other metals. Elemental mercury may be sprinkled in the home by Hispanic Americans who practice Santeria.

At room temperature, elemental mercury is a liquid. It volatilizes to a vapor that cannot be seen or smelled. When inhaled, elemental mercury vapor enters the blood, where it distributes primarily into red blood cells and the central nervous system. Because it is fun to play with, schoolchildren like to bring mercury home from science classes; if heated, inhalation may be dangerous.3738 Inhaling high levels of mercury vapor causes an acute, necrotizing bronchitis and pneumonitis. Deaths have resulted from heating elemental mercury in inadequately ventilated areas.37

The "Mad Hatter" in Alice in Wonderland suffered from the effects of exposure to mercury on the central nervous system. Mercury poisoning can sometimes be confused with a psychiatric illness because the patient may have insomnia, forgetfulness, loss of appetite, and a slight tremor. A patient with erethism from mercury poisoning characteristically has red palms, emotional lability, and memory impairment. Salivation and excessive sweating…

A tremendous amount has been learned about the effects of the environment on human health since World War II. We now have a far better understanding that exposures once thought to be innocuous, such as to cigarette smoke, mercury, and molds, may actually pose threats to children's health. However, we have a long way to go toward integrating this knowledge into clinical practice. One major reason why we have not managed to integrate environmental health into practice is that we know little about the specific environments our patients call home.

Before World War II, more than half of the patients who saw a physician saw him in their home. This allowed the physician to identify possible environmental risks and to provide appropriate advice about preventing disease. When the physician entered the patient's home, he would note characteristics such as the growth of mold on ceilings and walls and the presence of insects and rodents. If the physician's nose detected tobacco's familiar odor, he could counsel the smoker about the importance of quitting.

Because we no longer visit the patient's home, we usually have little understanding of the environment in which the family lives. There is a sort of paradox here: we now know far more about the effects of environmental factors on human health, but we know far less about the specific environments in which our patients live. One time-saving way to integrate environmental health into practice is to provide families with a short "home inventory" questionnaire to complete at the first office visit1,2 (Table 1).

Another substantial change in the past three decades is that levels of outdoor air pollution have fallen dramatically, whereas levels of indoor air pollution have risen. The levels of indoor air pollutants are higher because, after the energy crisis of the 1970s, Americans began building more airtight homes, increased their use of indoor space heaters, and opened fewer windows for ventilation. Four indoor air pollutants^ - carbon monoxide, environmental tobacco smoke, toxigenic molds, and mercury vapor - are among the most important to discuss with parents because they may lead to serious illness or death in some children. Each is addressed in this article, and advice is offered for anticipatory guidance. For more information, the reader is referred to the American Academy of Pediatrics Handbook of Pediatric Environmental Health, which contains guidance on these four indoor air pollutants and other environmental hazards for children.2

Table

TABLE 1Home Inventory Questionnaire

TABLE 1

Home Inventory Questionnaire

CARBON MONOXIDE

The most well-known of the fatal four indoor air pollutants is carbon monoxide (CO). Often called the "invisible killer," this gas has no color, odor, or taste. Children exposed to CO may have symptoms that mimic influenza.3-4 The most critical step for the pediatrician to suggest to the parent or guardian is that any child with suspected CO poisoning be immediately removed from the contaminated environment.

Children playing or sleeping in confined, poorly ventilated spaces such as garages, campers, and tents may be at risk for CO poisoning if fuel-powered equipment or charcoal grills are being used. Adolescents may be exposed to CO while working in and around cars and trucks when there is inadequate ventilation. Young children have died in the enclosed back of a pickup truck with a faulty exhaust system.

The relative affinity of CO for hemoglobin is approximately 240 times that of oxygen. The leftward shift of the oxyhemoglobin dissociation curve results in less oxygen delivery to the tissues. The carboxyhemoglobin (COHb) complex dissociates when the child is removed from the space contaminated with CO, and CO is excreted by the lungs. CO poisoning preferentially affects organ systems with high metabolic rates and high oxygen demand. Because of their higher metabolic rates, infants and children are more vulnerable to CO poisoning. When women are exposed to CO during pregnancy, less oxygen is available to the fetus. Fetal blood has a higher affinity for CO than adult blood and the fetus eliminates COHb slower than the adult.5-7 Thus, it is especially important to avoid exposure to CO during pregnancy.

Children with CO poisoning may complain of headache, dizziness, fatigue, weakness, drowsiness, nausea, and vomiting. The condition may be mistaken for viral illness. If the pediatrician or the parent suspects CO poisoning, prompt measurement of blood COHb is indicated. Physicians should be aware that the severity of the patient's symptoms may not correlate with the COHb level. Low levels of COHb may be found in patients with clinically severe symptoms.8

A high index of clinical suspicion is necessary to diagnose CO poisoning in children. Physicians should consider CO exposure when several household occupants have similar nonspecific symptoms. Because of their late onset, the characteristic signs of CO poisoning (eg, retinal hemorrhages and cherry-red mucosal membranes) are rarely observed on initial physical examination. Furthermore, measurements of oxygen saturation via pulse oximetry will be falsely normal because pulse oximetry cannot differentiate oxyhemoglobin from COHb. Arterial blood gas analysis is also misleading because the arterial oxygen tension (PaO2) is not affected by changes in hemoglobin saturation. Pediatricians should be aware that blood gas values may appear deceptively normal in CO poisoning.

An elevated level of COHb may confirm the diagnosis of CO poisoning, but low and moderately increased levels must be interpreted cautiously. Delay between exposure and laboratory measurement, treatment with oxygen, and other factors such as exposure to cigarette smoke should be considered when interpreting results. COHb levels in nonsmokers are usually 0.3% to 0.7%, whereas in smokers they range from 3% to 8%. COHb is eliminated in approximately 4 hours when room air is breathed and approximately 1 hour when 100% oxygen is breathed.

With hyperbaric oxygen, COHb is eliminated even more quickly (20 to 30 minutes), but there is no agreement among physicians that it is of benefit. Many experts use hyperbaric oxygen treatment only for pediatric patients with a COHb level greater than 25%; coma; a history of loss of consciousness; a history of cardiac arrest; or for pregnant women with CO poisoning.

To prevent CO poisoning, parents should be encouraged to take care in installing, maintaining, and using combustion appliances. The use of home CO detectors is not a substitute for yearly checks of fuel-burning appliances by a professional. CO detectors measure the amount of CO that has accumulated in the air and are set to alarm when CO in the air corresponds to a COHb level of 10% in the blood. They are not sensitive enough to detect lower levels of CO. Parents who purchase a CO detector should select one that has been certified by Underwriters Laboratories for home use.9

ENVIRONMENTAL TOBACCO SMOKE

The second of the fatal four indoor air pollutants is environmental tobacco smoke (ETS or second-hand smoke). ETS is composed of exhaled smoke and smoke released from the burning end of cigarettes, cigars, and pipes. There are more than 3,800 chemical compounds in ETS.

In the early 1990s, an estimated 43% of children 2 months to 11 years old lived in a home with at least 1 person who smoked cigarettes.10 Young infants who spend much of their time inside homes, child care settings, and vehicles may have more exposure to nicotine and the other chemicals in ETS than do older children.

Epidemiologic studies show that exposure to ETS increases a child's risk for a number of problems during childhood. It is a risk factor for sudden infant death syndrome.1112 Because of this clearly established association, it is important to remind parents who stopped smoking during pregnancy of the importance of continuing to keep the infant's home environment smoke-free during the first year of life.

The number of lower respiratory illnesses before the infant's first birthday increases in proportion to the number of smokers in the home. For example, hospitalization for pneumonia during the first year of life is 38% more likely in infants whose mothers smoke than in those whose mothers do not smoke. Moreover, the likelihood of hospitalization increases with the number of cigarettes the mother reports smoking daily.13,14 If both parents smoke, the infant is twice as likely as an infant whose parents are nonsmokers to have had pneumonia.15-17

Middle ear effusions are approximately 60% more likely among children whose parents smoke than among children whose parents do not smoke. An estimated 8% to 15% of middle ear effusions may be attributable to parental smoking.18

Asthma, the most common chronic disease of childhood, occurs more often among children whose mothers smoke cigarettes. Children with asthma have more frequent and severe asthma attacks when they live in a home where smoking occurs.19-21

Among adults, nonsmokers who live with smokers have lung cancer more often than do those who live with other nonsmokers. Children are more likely to have leukemia and lymphoma in adulthood if they are exposed to maternal smoking while in utero.22

When a child has a medical condition exacerbated by ETS exposure (eg, asthma or recurrent otitis media), parent education about the danger of smoking is a key element of that child's medical care. Smoking cessation counseling by physicians has been found to double smoking cessation; approximately 10% of smokers who are told to stop smoking by a physician do so.23 The pediatrician is often the only physician that parents of young children visit.24 Pediatricians therefore have an important role in helping to reduce the exposure of children to ETS.

TOXIGENIC MOLDS

The spores produced by toxigenic molds have emerged in the past 5 years as potentially dangerous indoor air pollutants. Toxigenic molds produce potent chemicals, known as mycotoxins. Toxigenic molds include Stachybotrys chartarum (also known as S. atra) and Trichoderma.

Common molds are ubiquitous in the outdoor environment, and can enter homes through doorways, windows, heating systems, ventilation systems, and air conditioning systems. The most common indoor molds are Cladosporium, Pénicillium, Aspergillus, and Alternaría.25 Most of these molds, typically found in showers or on items left too long in the refrigerator, do not produce mycotoxins.

All molds need water and nutrients to grow, but species of toxigenic molds have a higher water requirement than common household molds. Because of this, they tend to thrive only in places with chronic and severe water damage. Such water damage results from chronic leaks in roofs and walls, or from flooding. Toxigenic molds receive their nutrients from any source of cellulose (eg, wallpaper, wood, newspaper, or cardboard). They are thought to be uncommon in homes in the United States because of their higher water requirement, but no national survey has been done to determine their prevalence.

The toxic effects of exposure to molds must be differentiated from the allergic effects. Many pediatricians are familiar with the latter, characterized by persistent upper respiratory tract symptoms (eg, rhinitis, sneezing, and eye irritation) and lower respiratory tract symptoms (eg, coughing and wheezing).26-28

However, few pediatricians are familiar with the toxic effects of exposure to molds. The toxic effects seem to be due to inhalation of mycotoxins on the surface of the mold spores. These lipid-soluble toxins are readily absorbed by the lungs.29 Species of mycotoxin-producing molds include Fusarium, Trichoderma, and Stachybotrys. S. chartarum has been associated with acute pulmonary hemorrhage among young infants in Cleveland, Ohio,30"33 and Kansas City, Missouri,34 and with pulmonary hemosiderosis in a 7-year-old child in Houston, Texas.35 Trichoderma has been associated with life-threatening pulmonary hemorrhage in an infant visiting his grandfather's home in St. Louis.36 Although additional research is ongoing, it appears that the rapidly growing lungs of infants younger than 1 year may be especially vulnerable to the effects of certain mycotoxins, such as the trichothecene mycotoxins produced by Stachybotrys and Trichoderma.33 This may be because the trichothecenes, contained on the mold spores, are known to be potent protein synthesis inhibitors and this may result in pulmonary capillary fragility.

Several questions may help the pediatrician to identify mold problems in the home (Table 2). The best prevention strategy is to advise parents to clean up water and remove all water-damaged items (including carpets) within 24 hours of a flood or leak. If this is done, toxigenic molds, which usually take approximately 2 weeks to grow, will not have the opportunity to do so. If some mold is already present in the home, the water-damaged area needs to be washed with soap and water, followed with a solution of 1 part bleach to 4 parts water. Protective gloves should be worn during cleanup, because exposure of unprotected skin to toxigenic molds may cause a severe rash.

Table

TABLE 2Questions to Help Identify Mold Exposure

TABLE 2

Questions to Help Identify Mold Exposure

MERCURY VAPOR

Mercury vapor can be a fatal indoor air pollutant. Elemental mercury (quicksilver) is used in sphygmomanometers, thermometers, and thermostat switches. Dental amalgams contain approximately 50% mercury, as well as silver and other metals. Elemental mercury may be sprinkled in the home by Hispanic Americans who practice Santeria.

At room temperature, elemental mercury is a liquid. It volatilizes to a vapor that cannot be seen or smelled. When inhaled, elemental mercury vapor enters the blood, where it distributes primarily into red blood cells and the central nervous system. Because it is fun to play with, schoolchildren like to bring mercury home from science classes; if heated, inhalation may be dangerous.3738 Inhaling high levels of mercury vapor causes an acute, necrotizing bronchitis and pneumonitis. Deaths have resulted from heating elemental mercury in inadequately ventilated areas.37

The "Mad Hatter" in Alice in Wonderland suffered from the effects of exposure to mercury on the central nervous system. Mercury poisoning can sometimes be confused with a psychiatric illness because the patient may have insomnia, forgetfulness, loss of appetite, and a slight tremor. A patient with erethism from mercury poisoning characteristically has red palms, emotional lability, and memory impairment. Salivation and excessive sweating may occur. Mercury also accumulates in the kidney and may result in proteinuria or nephrotic syndrome.

Acrodynia (derived from the Greek for painful extremities) has occurred in infants after exposure to phenylmercury used as a fungicidal diaper rinse and in children exposed to mercury from interior latex paint.3940 The carbon-mercury chemical bond of phenylmercury is relatively unstable, so elemental mercury can be released from phenylmercury and inhaled and absorbed by the lung. This is why some interior latex paint, in which phenylmercury was used as a preservative until 1991, proved hazardous to young children. Mercury offgassing from painted walls was absorbed through the lungs and resulted in acrodynia in at least two children.39-40 Acrodynia has been mistaken for fifth disease, Kawasaki's disease, and measles because of the erythematous rash. Children with acrodynia may also have swollen and painful extremities, peripheral neuropathies, and hypertension.

If mercury poisoning is suspected, a 24-hour urine collection should be done. Normally, urinary mercury concentrations should be less than 10 to 20 ^g/L. However, if the mercury exposure is intermittent, the urinary mercury concentration does not necessarily correlate with the severity of toxic effects. Measurement of whole blood mercury is not useful because values tend to return to normal (< 0.5 to 1.0 pg/dL) within 1 to 2 days after the exposure to metallic mercury vapor ceases.

If mercury poisoning is diagnosed, it is crucial to identify the mercury source and end the exposure. If home exposure to mercury vapor is suspected, the child should be immediately removed from the contaminated environment. Some physicians use chelating agents to enhance mercury elimination, but whether chelation reduces toxic effects of mercury is unclear. Mercury poisoning should be treated in consultation with a physician who is trained in toxicology.

Currently, there is a national effort to reduce the use of elemental mercury. In hospitals and clinics, many mercury-containing oral thermometers and sphygmomanometers have been replaced with electronic equipment. However, mercury spills still occur. The amount of mercury in one thermometer is usually insufficient to produce clinically significant exposure in a child. Nevertheless, if a few drops of elemental mercury are spilled from the thermometer, it is important to advise the parents to handle it properly. A vacuum cleaner should not be used to clean up the mercury, as this disperses the droplets even more. Instead, the local health department should be called to obtain a mercury spill kit. If a large amount is spilled (eg, several cubic centimeters), the pediatrician should consult a certified environmental cleaning company. Concentrations of mercury vapor in the indoor air should not exceed 0.5 µg /m3.41,42

CONCLUSION

Each of the four indoor air pollutants mentioned in this article may cause fatalities in infants. It is important for pediatricians to be aware of each of them and to quickly remove infants from environments contaminated with these pollutants.

REFERENCES

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2. Etzel RA, Balk SJ, eds. American Academy of Pediatrics Handbook of Pediatric Environmental Health. Elk Grove Village, IL: American Academy of Pediatrics; 1999:22-23, 61-65, 97-98, 145-150.

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4. Heckerling FS, Leikin JB, Terzian CG, Maturen A. Occult carbon monoxide poisoning in patients with neurologic illness. Clin Toxicol. 1990;28:29-44.

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8. Conway EE. Recognizing carbon monoxide toxicity. Contemporary Pediatrics. 1994;11(suppl):24-32.

9. Underwriters Laboratories. UL2034: Standard for Single and Multiple Station Carbon Monoxide Detectors, 1st ed. Northbrook, IL: Underwriters Laboratories; April 30, 1992.

10. Pirkle JL, Flegal KM, Bernert JT, Brody DJ, Etzel RA, Maurer KR. Exposure of the US population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey, 1988 to 1991. JAMA. 1996;275:1233-1240.

11. Taylor JA, Sanderson M. A reexamination of the risk factors for the sudden infant death syndrome. J Pediatr. 1995;126:887-891.

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13. Colley JR, Holland WW, Corichili RT. Influence of passive smoking and parental phlegm on pneumonia and bronchitis in early childhood. Lancet. 1974;2:1031-1034.

14. Fergusson DM, Horwood LJ, Shannon FT. Parental smoking and respiratory illness in infancy. Arch Dis Child. 1980;55:358-361.

15. American Academy of Pediatrics, Committee on Environmental Health. Environmental tobacco smoke: a hazard to children. Pediatrics. 1997;99:639-042.

16. Harlap S, Davies AM. Infant admissions to the hospital and maternal smoking. Lancet 1974;1:529-532.

17. Rantakallio P. Relationship of maternal smoking to morbidity and mortality of the child up to the age of five. Acta Paediatr Scand. 1978;67:621-631.

18. Etzel RA, Pattishall EN, Haley NJ, Fletcher RH, Henderson FW. Passive smoking and middle ear effusion among children in day care. Pediatrics. 1992;90:228-232.

19. Chilmonczyk BA, Salmun LM, Megathlin KN, et al. Association between exposure to environmental tobacco smoke and exacerbations of asthma in children. N Engl J Med. 1993;328:1665-1669.

20. Martinez FD, Cline M, Burrows B. Increased incidence of asthma in children of smoking mothers. Pediatrics. 1992;89:21-26.

21. Weitzman M, Gortmaker S, Walker DK, Sobol A. Maternal smoking and childhood asthma. Pediatrics. 1990;85:505-511.

22. John EM, Savitz DA, Sandler DP Prenatal exposure to parents' smoking and childhood cancer. Am J Epidemiol. 1991;131:123-132.

23. Fiore MC, Bailey WC, Cohen SJ, et al. Smoking Cessation: Information for Specialists. Clinical Practice Guideline. Quick Reference Guide for Smoking Cessation Specialists, No. 18. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, Centers for Disease Control and Prevention; April 1996. Publication No. AHCPR 96-0694.

24. Perry CL, Silvis GL. Smoking prevention: behavioral prescriptions for the pediatrician. Pediatrics. 1987;79:790-799.

25. American Academy of Pediatrics, Committee on Environmental Health. Toxic effects of indoor molds. Pediatrics. 1998;101:712-714.

26. Dales RE, Zwanenburg H, Burnett R, Franklin CA. Respiratory health effects of home dampness and molds among Canadian children. Am J Epidemiol. 1991;134:196203.

27. Jaakkola JJK, Jaakkola N, Ruotsalainen R. Home dampness and molds as determinants of respiratory symptoms and asthma in pre-school children. Journal of Exposure Analysis and Environmental Epidemiology. 1993;3:129-142.

28. Verhoeff AP, van Strien RT, van Wijnen JH, Brunekreef B. Damp housing and childhood respiratory symptoms: the role of sensitization to dust mites and molds. Am J Epidemiol. 1995;141:103-110.

29. Croft WA, Jarvis BB, Yatawara CS. Airborne outbreak of trichothecene toxicosis. Atmospheric Environment. 1986,20:549552.

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31. Jarvis BB, Sorenson WG, Hintikka E-L, et al. Study of toxin production by isolates of Stachybotrys chartarum and Metnnoniella echinata isolated during a study of pulmonary hemosiderosis in infants. Appi Environ Microbiol. 1998;64:3620-3625.

32. Etzel RA, Montana E, Sorenson WG, et al. Acute pulmonary hemorrhage in infants associated with exposure to Stachybotrys atra and other fungi. Arch Pediatr Adolesc Med. 1998;152:757-762.

33. Dearborn DG, Yike I, Sorenson WG, Miller MJ, Etzel RA. Overview of investigations into pulmonary hemorrhage among infants in Cleveland, Ohio. Environ Health Perspect. 1999;107(suppl 3):495499.

34. Flappan SM, Portnoy J, Jones P, Barnes C. Infant pulmonary hemorrhage in a suburban home with water damage and mold (Stachybotrys atra). Environ Health Perspect. 1999;107:927-930.

35. Elidemir O, Colasurdo GN, Rossmann SN, Fan LL. Isolation of Stachybotrys from the lung of a child with pulmonary hemosiderosis. Pediatrics. 1999;104:964-966.

36. Novotny WE, Dixit A. Pulmonary hemorrhage in an infant following 2 weeks of fungal exposure. Arch Pediatr Adolesc Med. 2000;154:271-275.

37. Jaffe KM, Shurtleff DB, Robertson WO. Survival after acute mercury vapor poisoning. Am ] Dis Child. 1983;137:749-751.

38. Taueg C, Sanfilippo DJ, Rowens B, Szejda J, Hesse JL. Acute and chronic poisoning from residential exposures to elemental mercury: Michigan, 1989-1990. / Toxicol Clin Toxicol. 1992;30:63-67.

39. Hirschmann SZ, Feingold M, Boylen G. Mercury in house paint as a cause of acrodynia: effect of therapy with Nacetyl-D,L-penicillamine. N Engl J Med. 1963;269:889-893.

40. Agocs MM, Etzel RA, Parrish RG, et al. Mercury exposure from interior latex paint. N Engl ] Med. 1990;323:1096-1101.

41. Foote RS. Mercury vapor concentrations inside buildings. Science. 1972;177:513-514.

42. Agency for Toxic Substances and Disease Registry. Mercury toxicity. In: Agency for Toxic Substances and Disease Registry. Case Studies in Environmental Medicine, vol. 17. Atlanta, GA: U.S. Public Health Service, Agency for Toxic Substances and Disease Registry; March 1992.

TABLE 1

Home Inventory Questionnaire

TABLE 2

Questions to Help Identify Mold Exposure

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