Interior Surface Materials and Asthma in Adults: A Population-based Incident Case-Control Study

Abstract

The authors conducted a population-based incident case-control study to assess the relations between different types of interior surface materials and recent renovations at home and at work and the risk of asthma in adults. The authors systematically recruited all new cases of asthma during a 2.5-year study period (1997–2000) and randomly selected controls from a source population consisting of adults 21–63 years of age living in south Finland. The clinically diagnosed cases consisted of 521 adults with new asthma, and the controls consisted of 932 adults fulfilling eligibility criteria. In logistic regression analysis adjusting for confounding, the risk of asthma was related to the presence of plastic wall materials (adjusted odds ratio (OR) = 2.43, 95% confidence interval (CI): 1.03, 5.75) and wall-to-wall carpet at work (adjusted OR = 1.73, 95% CI: 0.74, 4.09), the latter in particular in the presence of mold problems (adjusted OR = 4.64, 95% CI: 1.11, 19.4). Use of floor-leveling plaster at home during the past 12 months was also a determinant of onset of asthma (adjusted OR = 1.81, 95% CI: 1.06, 3.08). These findings underline the need to consider the health aspects of materials used in floor, wall, and other indoor surfaces.

Working-age populations spend a lot of their time in different indoor environments; most of the time is spent in homes, and a substantial amount of time is spent in working environments, often indoors. The traditional design and construction of buildings are driven by functional, aesthetic, and economic values, but until recently little attention has been paid to the potential health impact related to indoor materials. The materials used in interior decoration, such as phthalates, other chemicals, and organic and inorganic particles, are potential sources of indoor air pollutants. Exposure to some of these compounds may induce harmful immunologic responses in the airways and increase the risk of bronchial hyperresponsiveness and asthma (1–5). Some compounds may be capable of producing irritant reactions in the airways, a route that could lead to irritant-induced asthma (6).

The textile surface materials used in wall-to-wall carpets, wallpapers, and furniture may emit chemical compounds, and they may serve as sources of particulate pollution. Danish and Finnish cross-sectional studies in office workers conducted in the late 1980s and early 1990s showed that mucosal symptoms are more common in offices with a large amount of textile surface materials (1, 2). Polyvinyl chloride materials are potential emission sources of the chemicals used as plasticizers, viscosity modifiers, and stabilizers in production, and such emissions usually take place for a long time. Epidemiologic studies carried out among child populations in Norway (3, 4), Finland (7), and Sweden (5) have shown relations between the amount of textile wall material and plasticized polyvinyl chloride materials at home and asthma, bronchial obstruction, and lower respiratory symptoms, but to our knowledge there are no reports on the potential effects of emissions from such building materials on adult-onset asthma. The potential of polyvinyl chloride products to cause asthma has been indicated in occupational settings in case reports among meat wrappers exposed to polyvinyl chloride film (8) and firefighters exposed to burning polyvinyl chloride (9). Renovation measures, such as painting, varnishing, gluing, and floor leveling, result in an increase in chemical emissions, which will then decline rather sharply over time. In a recent study of 5,951 Russian schoolchildren 8–12 years of age in nine cities, the risks of asthma, wheezing, and allergies were related to the installation of new linoleum flooring, synthetic carpet, wall covering, and particle board, as well as recent painting and the presence of new furniture (10).

We have previously reported that the risk of adult-onset asthma is related to the presence of visible mold and/or mold odor at work (11) and to pets at home in the past (12). There is some recent evidence that dampness may enhance the emissions from polyvinyl chloride materials and, thus, adverse respiratory effects. In a Swedish study of 87 employees in four geriatric hospitals, Norbäck et al. (13) found that asthma symptoms were more common in two buildings with signs of dampness. They suggested that this was related to degradation of di(ethylhexyl)phthalate in polyvinyl chloride floor material, since they measured increased levels of 2-ethyl-1-hexanol in indoor air reflecting degradation. We are not aware of any previous study investigating the joint effects of pets and carpet flooring on asthma, but we find it plausible that occupants of homes with pets and carpet flooring could experience more exposure to pet allergens than would occupants without pets and with other types of floors.

We studied the relations between different types of interior surface materials at home and at work and the risk of developing asthma in adulthood in a population-based incident case-control study of a working-age population. We also assessed the relations between renovations that had taken place in the home during the past 12 months and adult-onset asthma. In addition to assessing the independent effects of different surface materials, we evaluated the potential joint effects of mold problems and the presence of plastic floors or wall-to-wall carpet. Further, we tested a hypothesis that the presence of carpets will modify the effect of pets on the risk of adult-onset asthma.

MATERIALS AND METHODS

Study design

This study was a population-based case-control study of incident asthma. The source population consisted of adults 21–63 years of age living in the Pirkanmaa District, which is a geographically defined area in south Finland, with a population of 440,913 in 1997 (11, 12, 14). The ethics committees of the Finnish Institute of Occupational Health and the Tampere University Hospital approved this study, and participants gave a written, informed consent prior to participation.

Definition and selection of cases

We systematically recruited all new cases of asthma in the city of Tampere from September 1997 and in the whole Pirkanmaa Hospital District from March 1998 to April 2000. Patients were recruited at all health-care facilities diagnosing asthma, including the Department of Pulmonary Medicine at Tampere University Hospital, offices of pulmonary physicians in private practice in the region, and public health-care centers. As an additional route of case selection, the National Social Insurance Institution of Finland invited all patients who had received reimbursement rights for asthma medication during the study period and who had not yet participated.

The diagnostic criteria for asthma included occurrence of at least one asthma-like symptom and demonstration of reversible airways obstruction in lung function investigations, as shown in table 1. All the confirmed cases of asthma fulfilling the general eligibility criteria (residents aged 21–63 years of the Pirkanmaa District) were selected as cases. A total of 362 cases (response rate: 90 percent) participated through the health-care system and 159 cases through the National Social Insurance Institution (response rate: 78 percent), totaling 521 cases.

Selection of controls

Controls were randomly drawn from the source population by use of the national population registry, which has full coverage of the population, with the aim to recruit controls in a 2:1 ratio to cases. The general eligibility criteria were applied for controls. After up to three invitation letters and phone calls, 1,016 participated in the study (response rate: 80 percent). After exclusion of 76 subjects reporting previous or current asthma, six persons older than 63 years, and two persons returning incomplete questionnaires, our study population included 932 controls.

Exposure assessment

Exposure to emissions from interior surface materials was assessed by questionnaire information on the type of interior surface materials at home and at work. The following questions were asked:

• Is there wall-to-wall carpet/plastic floor material/textile wall material/plastic wall material in your home? (for each: no; yes, less than ½ of the floor/wall surface area; yes, at least ½ of the floor/wall surface area)

• Was your home renovated during the past 12 months? (yes; no)

• If yes, identify (painting, less than ½ of the wall surface area; painting, at least ½ of the wall surface area; wall papering, less than ½ of the wall surface area; wall papering, at least ½ of the wall surface area; varnishing/lacquering of the floor; use of floor plaster for leveling; other)

• Is there textile wall material/plastic wall material in your workplace? (for each: no; yes, less than ½ of the wall surface area; yes, at least ½ of the wall surface area)

• What is the floor material in your workplace? (concrete; wood; cork; plastic; wall-to-wall carpet; other; don't know)

Exposure to dampness and mold problems was assessed by questionnaire information on water damages, stains and other marks of structural dampness, visible mold, and mold odor both at home and indoors at work (11). Exposure to pets was assessed by questionnaire information on the presence of cat(s), dog(s), bird(s), rodent(s), or other hairy animals at home during the past 12 months and more than 12 months ago (12). The duration of pet keeping was also asked.

Data collection

At Tampere University Hospital, potential cases were recruited at their first visit due to suspected asthma, and the diagnosis was then verified in clinical examinations. At the other health-care facilities, cases were recruited immediately when the asthma diagnosis was confirmed. The National Social Insurance Institution invited cases from half a year to 2 years after their diagnosis was established. The date and criteria of their asthma diagnosis were confirmed from their medical records to ensure that their diagnosis fulfilled our criteria. Eligible subjects were invited to participate in the study by their physician or through a letter sent by the National Social Insurance Institution. Medical records of all cases were checked, and only those with no previously diagnosed asthma or long-term use of any asthma medication were included in the study. Recruitment of controls took place by a letter at regular intervals throughout the study period.

Measurement methods

All participants answered a self-administered questionnaire, modified from the Helsinki Office Environment Study questionnaire for use in a general population and described in detail in previous publications (11, 12, 14, 15).

For lung function measurements, the same diagnostic protocol was applied for all patients with suspected asthma (table 1) (11, 12, 16). The baseline spirometry and the bronchodilation test were recorded by a Medikro model 905 pneumotachograph spirometer with a disposable flow transducer (Medikro, Kuopio, Finland) connected to a computer according to standards of the American Thoracic Society (17). The presence of obstruction was judged by use of referent values derived from a Finnish population (18). All patients performed peak expiratory flow follow-up with measurements twice a day for at least 2 weeks using a mini-Wright meter. During the second week, measurements were taken before and 15 minutes after short-acting bronchodilating medication. A 2-week oral steroid treatment was carried out for those with a strong suspicion of asthma, if the other diagnostic tests were negative. The patient performed an additional 2 weeks of peak expiratory flow follow-up during this treatment and a spirometry test at the end of the treatment period to judge the response.

Statistical methods

We used the exposure odds ratio to quantify the relations between surface materials or renovation and the risk of asthma. We estimated the adjusted odds ratio in logistic regression analysis. Gender, age, education (as an indicator of socioeconomic status), personal smoking, and exposure to environmental tobacco smoke were systematically adjusted for as covariates. We also fitted parental atopy, other occupational exposures, and the age and type of building in the models, but because they had little influence on the studied relations they were not included in the final models. In addition, adjustment was made for the other exposure variables studied and shown in table 2.

We also studied the independent and joint effects of the two types of indoor environmental factors, that is, interior surface materials (either wall-to-wall carpet or plastic flooring) denoted as “A” and other indoor environmental factors (either mold problems or the presence of pets) denoted as “B,” by comparing the risk of asthma in four exposure categories: 1) no A and no B (reference category); 2) A and no B; 3) no A and B; and 4) A and B. We calculated odds ratios contrasting each of the three exposure categories to the reference category. Estimates for the independent effects of A and B and their joint effect were derived from the same logistic regression model adjusting for the covariates. For example, when the independent and joint effects of wall-to-wall carpet and molds were assessed, the regression model included the binary variables “wall-to-wall carpet only,” “molds only,” “both wall-to-wall carpet AND molds,” and all the covariates listed in table 3.

RESULTS

Characteristics of cases and controls

A larger proportion of cases than controls were women (⁠

= 24.6, p < 0.0001), in their twenties (⁠

\({\chi}_{1\mathrm{df}}^{2}\)

= 7.38, p = 0.007), current (⁠

\({\chi}_{1\mathrm{df}}^{2}\)

= 4.84, p < 0.028) or former (⁠

\({\chi}_{1\mathrm{df}}^{2}\)

= 2.64, p = 0.104) smokers, exposed to environmental tobacco smoke (at work or at home) (⁠

\({\chi}_{1\mathrm{df}}^{2}\)

= 2.42, p = 0.1197), and those with lower education (no vocational schooling or vocational course) (⁠

\({\chi}_{1\mathrm{df}}^{2}\)

= 15.3, p < 0.0001) (table 4). We adjusted for these factors in the multivariate analyses.

Surface materials and renovation in the home environment

Table 2 shows the occurrence of different home and workplace surface materials, as well as the experience and type of renovation in the home during the last 12 months, among cases and controls. It also presents crude and adjusted odds ratios of asthma in relation to exposure to different surface materials at home and through renovation. There were no statistically significant associations between the risk of asthma and the presence of any surface materials at home. The risk of asthma was slightly increased among subjects with plastic flooring, with an adjusted odds ratio of 1.17 (95 percent confidence interval (CI): 0.84, 1.62) for plastic on less than ½ and of 1.13 (95 percent CI: 0.85, 1.50) for plastic on ½ or more of the surface area.

Renovation that had taken place at home during the past 12 months was not related to an increased risk of asthma per se but, when looking at different types of renovation, use of plaster for floor leveling contrasted with no renovation was observed to significantly increase the risk of asthma, with an adjusted odds ratio of 1.81 (95 percent CI: 1.06, 3.08).

Surface materials in the work environment

Information on floor material in the work environment was collected in the six categories shown in table 2. The crude odds ratio for each specific type of floor material was calculated by the other types as the reference category. The adjusted odds ratios are from models that contrast plastic floor material and wall-to-wall carpet as the a priori hypothesized determinants to the remaining types of floor material, including concrete, wood, and cork, as the reference category. The adjusted odds ratio of asthma was 1.73 (95 percent CI: 0.74, 4.09) in relation to the presence of wall-to-wall carpet and 1.13 (95 percent CI: 0.84, 1.51) in relation to the presence of plastic flooring. The risk of asthma was also increased in relation to textile wall material on ½ or more of the surface area, with an adjusted odds ratio of 2.18 (95 percent CI: 0.77, 6.18) compared with no textile wall material. The effect estimate for the presence of either wall-to-wall carpet or textile wall material on over ½ of the surfaces at work was 1.78 (95 percent CI: 0.98, 3.17).

The risk of asthma was statistically significantly related to the presence of plastic wall material at work, with an odds ratio of 1.26 (95 percent CI: 0.49, 3.22) for plastic material on less than ½ of the surface and of 2.43 (95 percent CI: 1.03, 5.75) for plastic on ½ or more of the wall surface.

Joint effects of surface materials and other indoor environmental factors

Table 3 explores the independent and joint effects of wall-to-wall carpet and indoor mold problems, defined as the presence of visible mold or mold odor. The effect estimates for the independent effects of wall-to-wall carpet (adjusted odds ratio (OR) = 1.43, 95 percent CI: 0.69, 2.96) and mold problems (adjusted OR = 1.39, 95 percent CI: 0.91, 2.13) in the workplace were elevated, although the 95 percent confidence intervals included unity. The presence of both of these exposures simultaneously contrasted to none yielded an adjusted odds ratio of 4.64 (95 percent CI: 1.11, 19.4). The magnitude of the interaction on additive scale, that is, the additional effect above what is expected on the basis of the independent effects of the two factors, can be calculated as 282 percent (364 percent – 43 percent – 39 percent). The presence of both of these two exposures contrasted to one exposure (either carpet or mold) or no exposure yielded an adjusted odds ratio of 4.21 (95 percent CI: 1.01, 17.5).

The corresponding effect estimates for these exposures in the home environment were all lower with wider confidence intervals, but the pattern was similar with an increased odds ratio related to the presence of both wall-to-wall carpet and indoor mold. There was no evidence of a joint effect of plastic flooring and mold problems or wall-to-wall carpet at home and having pets currently or only more than 1 year ago (data not shown).

DISCUSSION

This study is to our knowledge the largest study addressing the determinants of clinically verified adult-onset asthma published to date. The incident case-control study design is very efficient compared with a cohort study needed to yield a similar amount of information. With our asthma incidence rate of 0.9 cases per 1,000 person-years, the present study corresponds to a follow-up of approximately 100,000 adults for approximately 5.8 years (the denominator was approximately 581,000 person-years). Our study provides new evidence that both plastic and textile surface materials in workplace indoor environments may play a role in the causation of asthma in adulthood. The risk of asthma was significantly related to the presence of plastic wall materials at work. The presence of both wall-to-wall carpet and textile wall materials at work increased the risk of asthma. The results showed a joint effect of a combination of wall-to-wall carpet and molds on the additive scale. In addition, use of plaster for floor leveling as part of renovation at home during the previous 12 months was a determinant of adult-onset asthma.

Validity of results

A thorough recruitment of new cases of diagnosed asthma in the health-care system with the help of the National Social Insurance Institution ensured that a high proportion of all new asthmatics in a geographically defined area participated in our study. The response rate among the control subjects was also relatively high. This excludes the possibility of any major selection bias.

Defining asthma on the basis of objective findings in extensive lung function measurements was performed to eliminate information bias concerning the outcome; that is, the knowledge of exposures of an individual did not affect the diagnosis. Such knowledge might cause bias when relying purely on physician-diagnosed asthma or on symptom reports.

Exposure assessment in the present study was based on reporting of potential sources of chemical and biologic indoor environmental exposures, including the type of flooring and wall covers as well as recent renovation activities. There has been some recent development in biomarkers of exposure to phthalates. Polyvinyl chlorides typically contain 30–40 percent di(2-ethylhexyl)phthalate (DEHP) by weight, and the primary metabolite of DEHP, mono-2-ethylhexyl phthalate (MEHP), and several other phthalate monoesters can now be measured from urine (19). However, the half-life of these urinary metabolites is short, and they reflect short-term exposure only, whereas questionnaire information on sources can elaborate longer exposure periods. In addition, urinary phthalate metabolites represent total exposure from inhalation, ingestion, and dermal contact, and phthalates are believed to come primarily from food and drink (20). Semivolatile phthalates migrate from floor materials to dust particles and can thus be measured in house dust (20–22), and the phthalate concentration in house dust has been used as a measure of exposure in one epidemiologic study (5). The results of a recent study showed no correlation between DEHP in house dust and DEHP metabolites in human urine (23). Both the urinary phthalate metabolite and dust phthalate concentrations are promising measures of exposure, but they need further development and are likely to be most useful in combination with questionnaire information on sources of exposure over time. Exposure assessment in the present study has some strengths that compensate for the lack of specific measurements of chemicals. The source-based exposure assessment used in the present study covers all potential causes leading to emissions. Information on the sources is expected to be comparable between cases and controls because, during the time of data collection, 1997–2000, there was little scientific evidence or public awareness of the potential role of surface material emissions or renovation in the development of asthma. Another strength of this study was that the majority of cases answered the questions on exposures before their asthma diagnosis was confirmed, which diminishes the potential influence of asthma diagnosis on reporting of exposures.

We were able to adjust for a number of potential confounders (refer to Materials and Methods) in logistic regression analysis in order to eliminate these factors as potential explanations for our results.

Synthesis with previous knowledge

Our findings on the relations between plastic and textile surface materials and the risk of asthma are consistent with four recent epidemiologic studies in children conducted in Norway (3, 4), Finland (7), Sweden (5), and Russia (10). In the first study (3), the risk of bronchial obstruction was greater in the presence of polyvinyl chloride in the floors (adjusted OR = 1.89, 95 percent CI: 1.14, 3.14) and in the presence of textile wallpaper in one or more rooms (adjusted OR = 1.58, 95 percent CI: 0.98, 2.54) compared with wood or parquet flooring and painted walls and ceilings. Further analyses showed that the relation of bronchial obstruction to a plasticizer exposure index was stronger in homes with low air change than in those with high air change (4). In a population-based cross-sectional study of 2,568 Finnish children aged 1–7 years, the risk of wheezing, persistent phlegm, weekly nasal congestion or excretion, and respiratory infections was related to the presence of plastic wall materials at home (7). In a case-control study of Swedish children aged 3–8 years, the risk of asthma was related to the house dust concentration of DEHP (5).

There are biologically plausible mechanisms that could explain the relation between plastic materials and the onset of asthma. Øie et al. (21) hypothesized that DEHP causes inflammation of the airways by mimicking some prostaglandins and thrombohexanes with a similar chemical structure. Larsen et al. (24, 25) studied the adjuvant effects of DEHP, MEHP, and other phthalate monoesters in a subcutaneous injection model with BALB/c mice. Ovalbumin was used as the model antigen, and ovalbumin-specific immunoglobulin E, immunoglobulin G₁, and immunoglobulin G_2a antibodies were measured as indicators of allergic response. MEHP produced a significant increase in the levels of both immunoglobulin E and immunoglobulin G₁, and DEHP increased immunoglobulin G₁ levels, these antibodies being related to a Th₂ response predominant in type I allergy. Some monophthalates have been shown to contribute to inflammatory processes by promoting cytokine interleukin 6 and interleukin 8 production in human epithelial cell line A549 (26).

Textile materials are potential sources of organic and nonorganic particles, as well as chemical emissions (27), which may cause inflammation of airways through allergic or irritative mechanisms. Besides the actual materials used in the production of textiles, particles attached to the surface may be resuspended and the chemicals adsorbed may be emitted into indoor air.

In the present study, the risk of asthma was not related to renovation in general or to painting, applying wall paper, varnishing, or lacquering in the home during the past 12 months, although all of these could result in chemical emissions. However, there was an increased risk of asthma related to the use of plaster for floor leveling. Floor plasters may contain potential sensitizers, such as casein, latex, and formaldehyde. Mäkinen-Kiljunen and Mussalo-Rauhamaa (28) reported high casein levels in Finnish house dust samples. They also measured the casein content of 27 pure plasters and found the highest level in a floor plaster (median: 2.4 μg/g; range: <0.1–8,300 μg/g).

In our study, the risk of asthma was related to the presence of plastic and textile materials in workplaces but not in homes. There are several possible explanations for the differences in the findings for homes and workplaces. The interior surface materials used in homes and workplaces may differ qualitatively within the exposure categories of “plastic” and “textile materials.” There may also be differences in temperature, relative humidity, ventilation rates, and airing through openable windows, which will lead to different levels of exposure by influencing either generation or removal of indoor pollution. Varying cleaning practices may also influence the differences in exposure levels. In general, occupants of homes have a greater influence on their home environmental conditions than do employees on their work environments, which may contribute to the heterogeneity of results from homes and workplaces.

Concluding remarks

This study provides new evidence that plastic and textile surface materials in workplaces may be related to increased risk of adult-onset asthma. In addition, the combined effect of wall-to-wall carpets and mold problems may be more than expected on the basis of their independent effects. Use of plaster for floor leveling at home was related to adult-onset asthma, while other renovation measures were not. These findings underline the need to consider the health aspects of materials used on floor, wall, and other surfaces in indoor environments.

The Ministry of Social Affairs and Health of Finland, the Finnish Work Environment Fund, and the West Midlands Regional Levy Board sponsored this study.

The authors would like to thank all the physicians and nurses who participated in recruiting the study subjects at the Tampere University Hospital, the health-care centers, and private practices. They would also like to thank the National Social Insurance Institution of Finland for providing the additional route of case recruitment and Dr. Ritva Piipari at the Finnish Institute of Occupational Health and Dr. Niina Jaakkola at the University of Helsinki for their contribution to the data collection and management.

Conflict of interest: none declared.

References