INDOOR AIR POLLUTANTS IN RESIDENTIAL SETTINGS:Respiratory Health Effects and Rem

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INDOOR AIR POLLUTANTS

IN RESIDENTIAL SETTINGS:

Respiratory Health Effects and

Remedial Measures to Minimize Exposure

2.3 Contaminants and Conditions

of Concern in Indoor Air

2.3.2 Mould

2.3.2.1 nature of the contaminant and its sources

Mould (a term used for microfungi) is most common in situations

where conditions indoors are very moist, either from condensation of

airborne water vapour on building surfaces (e.g. on or within

uninsulated walls), or from leakage of water, whether by rain or

runoff into the building or from pipes and taps inside the building.

(Johanning, 1998)

Mould spores are so small they cannot be seen except under a

microscope, and they are very light and travel on air currents.

Because mould spores are always present in outdoor air, they will

migrate indoors and be deposited on building material surfaces. If

the surfaces contain enough water, the spores will begin growing and

will be seen when the colony has developed mycelia (the " cottony "

growth characteristic of mould). The colony will produce more spores

which in turn will spread and colonize a larger surface area.

(Bartlett, 2001)

Dampness in buildings usually gives rise to the growth of a number

of different species of moulds simultaneously, and in fact,

exclusive exposure to any one mould, particularly the more toxic

varieties, is rare. (Johanning, 1998) In addition, different

building materials acquire a different repertoire of mould species

in the presence of moisture.

The following table lists the top 12 species of microfungi isolated

from North American wallboard. Fifty percent of the top 12 species

isolated are toxin producing. (, 1998)

Fungus

Chaetomium globosum

Penicillium viridicatum

Eurotium herbariorum

Penicillium aurantiogriseum

Penicillium citrinum

Stachybotrys chartarum

Aspergillus sydowii

Penicillium chrysogenum

Penicillium commune

Eurotrium repens

Memnoniella echinata

Aspergillus versicolor

% of 2134

wallboard samples

47.6

38.1

33.0

26.4

26.1

21.5

10.7

7.6

7.3

5.8

4.1

3.9

Different mould species have different requirements for the amount

of water necessary to grow. The species listed above cover a range

of possible water contents of colonized material. Some species

require very little moisture to grow; others require that the

building material be virtually water-saturated.

Studies at the Institute of Hygiene in Belgium revealed that the

sites more often contaminated in the home are: (Summerbell et al.,

1992)

kitchen and bath rooms (Cladosporium cladosporioides, Cladosporium

sphaerospermum, Ulocladium botrytis, Chaetomium globosum,

Aspergillus fumigatus)

wallpaper (C. spaerospermum, Chaetomium species, Doratomyces

species, Fusarium species, Stachybotrys atra, Trichoderma species,

Scopulariopsis species)

mattresses, carpets (Penicillium species, Aspergillus versicolor,

Aureobasidium pullans, Aspergillus repens, Wallemia sebi, Chaetomium

species)

window-frames (A. pullulans, C. sphaerospermum, Ulocladium species)

cellars and crawl spaces (A. versicolor, A. fumigatus, Fusarium

species)

the soil of ornamental plants (A. fumigatus, Aspergillus niger,

Aspergillus flavus)

insulation material (A. versicolor, A. fumigatus, Fusarium species).

A Belgian study of 130 homes over a 10-year period ranked mould

growth by species in indoor environments. The ten most common

species were Cladosporium, Penicillium, Aspergillus, Aureobasidium,

Scopulariopsis, Alternaria, Acremonium, Ulocladium, Mucor, and

Rhizopus species. (Beguin & Nolard, 1994)

In a Danish study of 72 mould-contaminated building materials from

23 buildings suffering from water damage, the microfungal genera

most frequently encountered were Penicillium (68%), Aspergillus

(56%), Chaetomium (22%), Ulocladium (21%), Stachybotrys (19%) and

Cladosporium (15%). Penicillium chrysogenum, Aspergillus versicolor,

and Stachybotrys chartarum were the most frequently occurring

species. (Gravesen et al., 1999)

One species that has received considerable attention is Stachybotrys

Chartarum. Stachybotrys chartarum is a type of mould that can

potentially produce potent mycotoxins. It has been implicated

recently in episodes of human illness in both housing and portable

school classrooms. In a study listing moulds most frequently

isolated from the air of 47 dwellings in Central Scotland,

Stachbotrys was found in 12.8% of dwellings, and ranked 16th among

the top 19 species. (Hunter et al., 1988)

Specific identifiable components within certain moulds can adversely

affect human respiratory health. For example, the compound (1® 3)-b-

d-glucan is a major structural component of almost all fungal cell

walls. (Summerbell, 1998) A study in Erfurt and Hamburg, Germany,

demonstrated the following associations between significant

increases in (1® 3)-b-d-glucan levels and the following housing

characteristics:

Carpets in the living room (means ratio (MR) 1.9-2.1)

Keeping a dog inside (MR 1.4)

Use of the home by four or more persons (MR 1.4)

Lower frequency of vacuum cleaning (MR 1.6-3.0)

Lower frequency of dust cleaning (MR 1.4)

Presence of mold spots during the past 12 months (MR 1.4).

The researchers also found that the (1® 3)-b-d-glucan concentrations

in house dust, measured in mg/m2, are also correlated with levels of

endotoxins, allergens and culturable mold spore counts in house

dust. (Gehring et al., 2001)

2.3.2.2 selected evidence suggesting adverse respiratory effects

Asthma

In Kilpelainen's study of Finnish university students cited earlier,

the strongest association discovered was between exposure to visible

mould and asthma. (Kilpelainen et al., 2001)

Norback and colleagues, in the study on building dampness cited

earlier, also showed that immediate type allergy to moulds

(Cladosporium and Alternaria) was more prevalent in damp dwellings

(9.3% incidence vs. 3.9%). Further, they demonstrated that the mould

allergy was associated with current asthma (odds ratio 3.4,

confidence interval 1.4-8.5). (Norback et al., 1999)

A study by Taskinen and colleagues in eastern Finland compared

schools with moisture and mould problems to a reference school.

Their results demonstrated an association between the presence of

moulds, atopic allergy to these moulds, and asthma or asthma-like

conditions. All the children with skin prick test reactions to

moulds reacted to at least one of the moulds used to indicate

dampness (Fusarium roseum, Aspergillus fumigatus, Phoma herbarum or

Rhodotorula rubra). The presence of these moulds was a criterion for

choosing problem buildings. All the reactive children had either

asthma or wheezing. (Taskinen et al., 1997)

Respiratory Symptoms

In a Canadian study of some 14,799 adults at least 21 years of age,

questionnaires were administered to investigate the association

between home dampness and mold and health. The presence of home

dampness and/or molds was reported by 38% of respondents. The

prevalence of lower respiratory symptoms (any cough, phlegm, wheeze,

or wheeze with dyspnea) was increased among those reporting dampness

or mould compared with those not reporting dampness or mould. The

authors concluded that exposure to home dampness and mould is a risk

factor for respiratory disease in the Canadian population. (Dales et

al., 1991a)

A review of nine population-based studies indicated one or more

positive associations between mould levels and health outcomes as

measured by symptoms of respiratory disease in seven of the nine

cross-sectional studies identified. The studies also indicated that

dampness and mold problems are present in 20% to 50% of modern

homes. The authors concluded that moulds do contribute to allergic

disease, and the extent of their involvement is probably greater

than is indicated by the available clinical and epidemiologic

studies. (Verhoeff & Burge, 1997)

In a study of Finnish flats and terraced houses, occupants were

compared for respiratory symptoms between homes with visible mould

growth and those without a mould problem. The occurrence of

respiratory symptoms (including rhinitis, sore throat, hoarseness,

cough, phlegm, tight chest, dyspnea, and wheezing) was significantly

higher in the exposed group than in the non-exposed. Cough and

dyspnea were relieved in most cases during interruption of exposure

(e.g. on vacations). Symptoms of chronic bronchitis were

significantly more common in the exposed group (odds ratio 3.4, 95%

confidence interval 1.1-10.9), when adjusted for age, sex, atopy and

smoking. (Husman et al., 1993)

In a more recent study, exposure to mould was significantly

associated with cough without phlegm, nocturnal cough, sore throat,

rhinitis, fatigue and difficulties in concentration. While this type

of association between respiratory infections and exposure to

moisture or mould has previously been reported for children, the

finding for adults is new. (Koskinen et al., 1999)

In an attempt to generate more definitive data on health effects of

mouldy buildings, one research group undertook nasal lavage fluid

analysis to determine whether inflammatory markers showed changes in

persons exposed to mouldy buildings. Their results comparing a mould-

exposed and a reference group indicated an association between

inflammatory markers in the nasal lavage fluid, the high prevalence

of respiratory symptoms among the occupants (such as cough, phlegm

production and rhinitis), and chronic exposure to moulds in the

indoor environment. (Hirvonen et al., 1999)

Dales et al. attempted to confirm by objective measures whether the

associations that have hitherto been detected using questionnaires

were supportable by measurement. Quantitative and qualitative mould

measures (airborne ergosterol and viable microfungi in dust) were

compared to respiratory symptoms and nocturnal cough recordings in

Canadian elementary school children during the winter of 1993-1994.

There was a 25-50 percent relative increase in symptom prevalence

when mould was reported to be present (p < 0.05). But neither

symptoms nor recorded cough was related to objective measures of

mould. The researchers conclude that either these objective measures

or the traditionally used questionnaire data are inaccurate, and

that this discrepancy limits the acceptance of a causal relation

between indoor microfungal growth and illness. (Dales et al., 1999)

Douwes and colleagues evaluated the use of extracellular

polysaccharides of Aspergillus and Penicillium mould species (EPS-

Asp/Pen) in house dust as a marker for mould exposure, and in turn

studied the relation between EPS-Asp/Pen levels and home dampness

and respiratory symptoms in children. They found that EPS-Asp/Pen

levels in living room floor dust were positively associated with

occupant-reported home dampness, and with respiratory symptoms.

(Douwes et al., 1999)

Airborne (1® 3)-b-d-glucan was measured in buildings in which

complaints of eye and airway irritation as well as fatigue and skin

symptoms had been numerous. The presence of symptoms was evaluated

using questionnaires. Dose-response relationships were found between

levels of (1® 3)-b-d-glucan and eye and throat irritation, dry cough

and itching skin. (Rylander et al., 1992)

Common Cold and Other Respiratory Infections

The study of Finnish flats and houses by Husman et al. also found

that the percentage of adults who had at least one acute respiratory

infection during the previous 12 months was significantly higher in

the mould-exposed group than in the non-exposed. The risk of acute

respiratory infections associated with the exposure was 2.2 (95%

confidence interval 1.2-4.4) when adjusted for age, sex, smoking and

atopy. Schoolchildren in problem dwellings had recurrent respiratory

infections requiring antibiotic treatment (e.g. tonsillitis,

sinusitis, and acute bronchitis) more often than their non-exposed

references. The occurrence of all respiratory infections in children

under seven years was significantly higher in the study group than

in the reference group. (Husman et al., 1993)

Kilpelainen's study of Finnish university students cited earlier

also found an association between exposure to visible mould and

common colds. (Kilpelainen et al., 2001) Koskinen et al. also

reported a significant association between exposure to mould and the

common cold. (Koskinen et al., 1999)

Airway Inflammation

In an animal study, acute inflammatory response in the lungs was

studied in guinea pigs after a single inhalation exposure of (1® 3)-

b-d-glucan. In the water insoluble form, (1® 3)-b-d-glucan caused a

delayed response in terms of a decrease in macrophages and

lymphocytes in the lung wall, 1 to 7 days after exposure. (Fogelmark

et al., 1992)

A later paper reviewed field studies in which (1® 3)-b-d-glucan was

measured as a marker of biomass and was related to the extent of

symptoms and measures of inflammation among exposed subjects.

Increased levels of (1® 3)-b-d-glucan were related to an increased

extent of symptoms and markers of inflammation. The data suggest

that (1® 3)-b-d-glucan can be used as a risk marker in indoor

environments. " (Rylander, 1999 and 2000)

Laboratory studies are also supportive of an association between (1®

3)-b-d-glucan and activation of pulmonary alveolar macrophages

(PAMs), possibly making the lungs hyperreactive to a wide variety of

foreign materials. (Summerbell, 1998) Fungal glucan decreases

phagocyctosis and decreases pulmonary alveolar macrophage numbers

( and Day, 1997) Also, in double-blind inhalation exposure

trials conducted with human volunteers, exposure to (1® 3)-b-d-

glucan correlated significantly with some non-specific respiratory

symptoms. The most strongly correlating symptom was headache.

(Summerbell, 1998)

Pulmonary alveolar macrophage function and the immune system

response to (1® 3)-b-d-glucan are only partially understood. It

appears that exposure causes inflammatory changes in lymphocytes,

decreases lymphocyte mitogenicity and interleukin-1 (IL-1) secretion

(via T-cells) and stimulates bacterial and tumor defences. (

and Day, 1997)

Lung Function

Peak expiratory flow (PEF) variability was investigated in 148

children 7 to 11 years of age, of whom 50% had self- or parent-

reported chronic respiratory symptoms. Endotoxin and (1® 3)-b-d-

glucan were measured in dust extracts. The levels of (1® 3)-b-d-

glucan per square meter of living room floor were significantly

associated with peak flow variability, particularly in atopic

children with asthma symptoms. No associations were found with

endotoxin levels, or for levels of either microbial agent and

bedroom floor or mattress dust. (Douwes et al., 2000)

Ideopathic Pulmonary Haemorrhage and Pulmonary Hemosiderosis

At very high exposure levels to specific moulds, nose bleeding,

hemoptysis, and pulmonary haemorrhage have been documented.

(Rylander & Etzel, 1999)

A geographic cluster of 10 cases of pulmonary haemorrhage and

hemosiderosis in infants occurred in Cleveland, Ohio, between

January 1993 and December 1994. An early study into the cases

observed a greater frequency of water damage in homes of affected

infants compared to those of controls. (Montaña et al., 1997) The

finding of water damage led to air and surface sampling for mold,

which revealed heavier growth of several fungi in case homes. The

toxigenic fungus Stachybotrys chartarum was found in almost all of

the case homes studied and about half of the control homes.

(Dearborn, 1997) However, the causal connection between Stachybotrys

chartarum exposure and respiratory illness has not been well

established, because it has not been studied in the absence of other

mould exposures.

A community-based control study was undertaken to test the

hypothesis that the 10 infants were more likely to live in homes

where Stachybotrys chartarum was present than were 30 age-matched

and ZIP code-matched control infants. (Etzel et al., 1998) The

infants' home environments were investigated using biosampling

methods with specific attention to Stachybotrys chartarum, and air

and surface samples were collected from the room where the infant

was reported to have spent the most time.

Viable Stachybotrys spores were detected in filter cassette samples

of the air in homes of 5 of 9 patients, and 4 of 27 controls. The

mean concentration of Stachybotrys chartarum was 43 CFU/m3 in homes

of patients vs. 4 CFU/m3 in homes of controls when averaged across

all media. The mean concentration of Stachybotrys chartarum on

surfaces was 20 x 106 CFU/g and 0.007 x 106 CFU/g in homes of

patients and controls, respectively. Other funguses such as

Aspergillus, Cladosporium, and Penicillium were also identified,

with mean CFU counts for all fungi averaging 29,227 CFU/m3 in homes

of patients vs. 707 CFU/m3 in those of controls. The researchers

concluded:

" Infants with pulmonary haemorrhage and hemosiderosis were more

likely than controls to live in homes with toxigenic Stachybotrys

[chartarum] and other fungi in the indoor air. " (Etzel et al.,

1998).

Between 1993 and 1998, a total of 37 cases of pulmonary haemorrhage

and hemosiderosis were identified in the Cleveland vicinity,

including the initial cluster of ten cases. Twelve of the infants

have died, including seven who were originally were identified as

sudden infant death syndrome. Thirty of these cases were African

American children who lived within a contiguous nine zip code area

in the eastern part of the metropolitan area. This residential area

contains primarily wood frame homes, most of which were more than 60

years old. The area is a drainage plain where basements are

frequently flooded in heavy rainstorms. The forced air heating in

these homes commonly draws air from the entire basement, providing a

means for airborne particulates to be circulated up into the

infants' sleeping areas. (Dearborn et al., 1999)

Researchers at the Texas Children's Hospital treated a seven-year

old boy who had been asymptomatic until his family moved into a 25-

year old farmhouse that had suffered from severe flood damage and

was being reconstructed in stages. Bronchoalveolar lavage (BAL)

fluid showed a moderate number of hemosiderin-laden macrophages

(26%), indicating intrapulmonary bleeding, and grew Stachybotrys

chartarum in Sabouraud-dextrose agar medium. Multiple cultures in

the home grew Stachybotrys chartarum, and Aspergillus and

Penicillium species were also recovered. The researchers concluded:

" In summary, we report the first isolation of Stachybotrys atra from

the BAL fluid of a child with PH [pulmonary hemosiderosis]. The

isolation of the organism from the patient's water-damaged home and

the resolution of symptoms after his move to another home provide

additional evidence that environmental exposure to Stachybotrus atra

was responsible for the patient's pulmonary disease. Although the

focus has previously been on Stachybotrys atra and infants with PH,

our case demonstrates that Stachybotrys atra is also associated with

PH in older children. " (Elidemir et al., 1999)

While the physical evidence in the water-damaged home indicates that

Stachybotrys was present in conjunction with other molds, the case

study reports only the culture of Stachybotrys in the BAL fluid. The

published documentation was not sufficient to determine whether

other species had also been cultured in the BAL fluid. The authors

do indicate that they failed to find sources of contamination from

the equipment used during and after the bronchoscopy, suggesting

that growth of Stachybotrys in the BAL fluid did indeed represent

actual recovery of Stachybotrys spores from the patient.

A review within the Center for Disease Control (CDC) and by outside

experts of an investigation of acute pulmonary

haemorrhage/hemosiderosis in infants identified shortcomings in the

implementation and reporting of the investigation. The reviews led

CDC to conclude that a possible association between acute pulmonary

haemorrhage and hemosiderosis in infants and exposure to molds,

specifically Stachybotrys chartarum, was not proven. (CDC, 2000)

2.3.2.3 summary of selected evidence

The evidence cited suggests an association between mould exposure in

housing and various adverse respiratory health effects, including:

exacerbation of asthma

development of allergy to mould

increased incidence of wheezing and other respiratory symptoms

increased incidence of upper respiratory infections

inflammation of the airways

changes in lung function, e.g. increased peak flow variability

ideopathic pulmonary haemorrhage

Mould appears to exacerbate respiratory conditions both directly

(e.g. exacerbation of existing asthma) and indirectly (e.g.

increased incidence of colds and increased sensitization).

To evaluate the health consequences for children of indoor exposure

to moulds, an international workshop was organized with 15

scientists from 8 countries in andria, Virginia, April 21-24,

1998. The participants agreed that exposure to moulds constitutes a

health threat to children resulting in respiratory symptoms in both

the upper and lower airways, an increased incidence of infections,

and skin symptoms. Allergy, either to moulds or to other indoor

agents, also presents a health risk. (Rylander & Etzel, 1999).

With respect to exposures to specific toxic moulds, the consensus is

more cautious about specific conclusions. For example, in the wake

of the Cleveland cases, the American Academy of Pediatrics published

guidelines in 1998 for pediatricians concerning toxic mold exposures

in children. It is interesting that their approach invokes

the " precautionary principle " :

" Very little is currently known about acute idiopathic pulmonary

haemorrhage among infants. This is a newly recognized problem and

knowledge is expected to be evolving rapidly. In view of the

severity of the problem, environmental controls to eliminate water

problems and to reduce the growth of indoor molds are wise. Until

more is known about the etiology of idiopathic pulmonary

haemorrhage, prudence dictates that pediatricians try to ensure that

infants under 1 year of age are not exposed to chronically moldy,

water-damaged environments. " (American Academy of Pediatrics, 1998)

The study of a seven-year old boy with pulmonary hemosiderosis (PH)

cited earlier led researchers to recommend that the American Academy

of Pediatrics recommendations on mold exposure should include all

children with PH, not just infants. (Elidemir et al., 1999)

2.3.2.4 remedial action to avoid exposure

In terms of practical response and recommendations for physical

changes to reduce illness, some agencies have recommended

remediation to remove moulds. For example, a special Toxic Fungi

Abatement Workshop was held at Case Western Reserve University in

Cleveland, Ohio in March, 1996, to initiate a program to prevent

pulmonary hemosiderosis in infants. The working group of scientists

and public officials at the Workshop concluded that pulmonary

hemosiderosis detected in infants in a specific locality in

Cleveland was most likely explained by high exposure to mycotoxins

in the spores, mycelia and substrate dusts from Stachybotrys

chartarum. Given this conclusion, the working group refined a

prevention program designed to detect homes of infants that might be

at high risk, and to test these homes for Stachybotrys chartarum to

ascertain the safety of the infant remaining in the home and to

guide the extent of abatement necessary. (Cuyahoga County Board of

Health et al., 1996) As discussed above, the Center for Disease

Control no longer concludes that there is any proven relationship

between Stachybotrys chartarum and pulmonary haemorrhage and

hemosiderosis. (CDC, 2000)

In addition, the New York City Department of Health promulgated

guidelines on assessment and remediation of Stachybotrys chartarum

in indoor environments. They emphasize that prompt removal of

contaminated material and infrastructural repair must be the primary

response to Stachybotrys chartarum contamination in buildings. They

state that contamination should be prevented by proper building

maintenance and prompt repair of water damaged areas. (New York City

Department of Health, 1996) Since then, a new and broader New York

protocol inclusive of all fungi has been issued,

entitled " Guidelines on Assessment and Remediation of Fungi in

Indoor Environments " . (New York City Department of Health, 2000)

In general, the environmental remedies most often chosen to reduce

health effects from microbiological contaminants are:

Remediate moisture damage by remedying the cause and removing mould

and mouldy materials

Eliminate standing water in ventilation or humidification systems

Improve building drainage to eliminate water flow into basements

Improve building envelopes to reduce air infiltration/exfiltration

and water leakage

Introduce sufficient local and general ventilation to keep rooms dry

(e.g. bathroom)

Canada Mortgage and Housing Corporation (CMHC) undertook a limited

pilot study to assess the degree of improvement that might be

available to asthmatic homeowners who undertook renovations to

eliminate sources of indoor pollutants or mould. Five households

with at least one asthmatic family member in each joined the

remediation study. Improvements in the asthma condition of the

occupants correlated with the degree of improvement of the air

quality of the house after remediation (e.g. reduction in mould

detected in basements). Of the five homes, the adult asthmatic of

House 1 did not find any improvement; the asthma of the owner of

House 2 became worse while he gutted his basement; both daughter and

mother in House 3 experienced significant improvement of asthma and

chronic fatigue symptoms, respectively, after the renovation; and

the adult asthmatics of Houses 4 and 5 reported marked improvement

and no longer needed medication half a year to nine months after the

renovation. (Canada Mortgage and Housing Corp., 1999)