Skip to main content

Main menu

  • Home
  • Current issue
  • Past issues
  • Authors/reviewers
    • Instructions for authors
    • Submit a manuscript
    • COVID-19 submission information
    • Institutional open access agreements
    • Peer reviewer login
  • Alerts
  • Subscriptions
  • ERS Publications
    • European Respiratory Journal
    • ERJ Open Research
    • European Respiratory Review
    • Breathe
    • ERS Books
    • ERS publications home

User menu

  • Log in
  • Subscribe
  • Contact Us
  • My Cart

Search

  • Advanced search
  • ERS Publications
    • European Respiratory Journal
    • ERJ Open Research
    • European Respiratory Review
    • Breathe
    • ERS Books
    • ERS publications home

Login

European Respiratory Society

Advanced Search

  • Home
  • Current issue
  • Past issues
  • Authors/reviewers
    • Instructions for authors
    • Submit a manuscript
    • COVID-19 submission information
    • Institutional open access agreements
    • Peer reviewer login
  • Alerts
  • Subscriptions

Volatile organic compounds and risk of asthma and allergy: a systematic review

Ulugbek B. Nurmatov, Nara Tagiyeva, Sean Semple, Graham Devereux, Aziz Sheikh
European Respiratory Review 2015 24: 92-101; DOI: 10.1183/09059180.00000714
Ulugbek B. Nurmatov
1Allergy and Respiratory Research Group, Centre for Population Health Sciences, The University of Edinburgh, Medical School, Edinburgh, UK
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • For correspondence: Ulugbek.Nurmatov@ed.ac.uk
Nara Tagiyeva
2Division of Applied Health Sciences, University of Aberdeen, Aberdeen, UK
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Sean Semple
2Division of Applied Health Sciences, University of Aberdeen, Aberdeen, UK
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Graham Devereux
2Division of Applied Health Sciences, University of Aberdeen, Aberdeen, UK
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Aziz Sheikh
1Allergy and Respiratory Research Group, Centre for Population Health Sciences, The University of Edinburgh, Medical School, Edinburgh, UK
3Division of General Internal Medicine and Primary Care, Brigham and Women's Hospital, Boston, MA, USA
4Harvard Medical School, Boston, MA, USA
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF
Loading

Abstract

Volatile organic compounds (VOCs) are ubiquitous domestic pollutants. Their role in asthma/allergy development and exacerbations is uncertain. This systematic review investigated whether domestic VOC exposure increases the risk of developing and/or exacerbating asthma and allergic disorders.

We systematically searched 11 databases and three trial repositories, and contacted an international panel of experts to identify published and unpublished experimental and epidemiological studies.

8455 potentially relevant studies were identified; 852 papers were removed after de-duplication, leaving 7603 unique papers that were screened. Of these, 278 were reviewed in detail and 53 satisfied the inclusion criteria. Critical appraisal of the included studies indicated an overall lack of high-quality evidence and substantial risk of bias in this body of knowledge. Aromatics (i.e. benzenes, toluenes and xylenes) and formaldehyde were the main VOC classes studied, both in relation to the development and exacerbations of asthma and allergy. Approximately equal numbers of studies reported that exposure increased risks and that exposure was not associated with any detrimental effects.

The available evidence implicating domestic VOC exposure in the risk of developing and/or exacerbating asthma and allergy is of poor quality and inconsistent. Prospective, preferably experimental studies, investigating the impact of reducing/eliminating exposure to VOC, are now needed in order to generate a more definitive evidence base to inform policy and clinical deliberations in relation to the management of the now substantial sections of the population who are either at risk of developing asthma/allergy or living with established disease.

Abstract

Investigation of VOCs in relation to developing or exacerbating asthma or allergy indicates new studies are required http://ow.ly/wEJ19

Introduction

In westernised countries, asthma and allergic diseases are a public health concern because of their high prevalence, associated morbidity and substantial healthcare and societal costs [1, 2]. The prevalence of asthma and allergic disorders has increased since the early 1960s [3–12] and, although it is generally accepted that changes in the prevalence are a consequence of changing environmental influences, the identities of the relevant environmental exposures remain unclear.

Volatile organic compounds (VOCs) are important indoor air pollutants produced by evaporation at room temperature from paints, wood, fabrics, cleaning agents, air fresheners, cosmetics, furnishings and floor and wall coverings. Indoor VOC levels exceed those outdoors [13–15], and are further increased by cigarette smoking and if a garage is attached to a house [16]. Greater use of VOC-containing products has, together with more effective insulation and less external ventilation of modern buildings, contributed to increased VOC exposure. The possible health effects of indoor VOC exposure are a cause for concern, given that people in general, and children in particular, now spend most of their time indoors [14, 17].

Several developments have led to a renewed interest in the possible effects of residential VOC exposure on asthma/allergy. These include the development of technologies that facilitate the quantification of individual VOC exposure, longitudinal cohort studies reporting associations consistent with a link between antenatal VOC exposure and childhood asthma/allergy [18, 19], and new approaches to reducing residential VOC exposure. Interventions to reduce VOC exposure are now feasible by, for example, avoiding redecoration, new furniture, air fresheners and perfumed items, and increasing ventilation [16]. The technology now also exists to construct so-called “nontoxic” houses, which are built without unplasticised polyvinyl chloride (uPVC) frames and using low-VOC paints and coverings.

We report here a systematic review investigating the possible effects of domestic VOC exposure on the development of asthma/allergy and the impact of VOCs on those with established disease.

Methods

We searched the following 11 international databases using a detailed search strategy (supplementary material, appendix 1): MEDLINE (1966–2012), EMBASE (1980–2012), Cochrane Library (1992–2012), LILACS (1986–2012), ISI Web of Science (1970–2012), BIOSIS (1969–2012), Global Health (1987–2012), AMED (1985–2012), TRIP (2003–2012), CAB (1910–2012) and CINAHL (1937–2012). Unpublished data and research in progress were identified using the key Internet-based databases www.clinicaltrials.gov, www.controlled-trials.com and www.anzctr.org.au, and by contacting international experts in the field (supplementary material, appendix 2). The bibliographies of included studies were scrutinised to identify further relevant studies. There were no language restrictions.

Observational studies (cross-sectional, case–control and cohort) and intervention studies (randomised controlled trials (RCTs), quasi-RCTs, controlled clinical trials (CCTs), controlled before-and-after (CBA) studies and interrupted time series) were eligible for inclusion; case reports/series and expert opinions were excluded.

Papers were included if they investigated the role of domestic (e.g. home, school, day care), objectively measured airborne exposure to VOCs occurring in real-life indoor environments, in the development of asthma/allergy and/or in exacerbating established disease. We therefore excluded papers reporting exposure to VOC sources, modelled or estimated exposure, and experimental exposure under laboratory conditions. Studies reporting only on exposure biomarkers were excluded on the grounds of their wide inter- and intra-individual variability, potential biological instability and because these measures reflect endogenous metabolites and routes of exposure, including those outside the scope of this review (e.g. digestive, dermal) (supplementary material, appendix 3). We also excluded studies that measured residential VOC concentrations to quantify exposure to environmental tobacco smoke.

Included studies reported ante- and post-natal exposures and outcomes in children and adults. The main outcomes of interest were: the incidence or prevalence of asthma, atopic eczema/dermatitis and allergic rhinitis/rhino-conjunctivitis; and evidence of allergic sensitisation. Secondary outcomes of interest were measures of increased disease activity by any objective measure (e.g. lung function, symptom scores, exacerbations, medication usage, healthcare utilisation and quality of life). Studies that reported nonspecific symptoms, such as throat/nasal irritation and symptoms associated with sick building syndrome, were excluded.

Two researchers independently reviewed titles and abstracts of identified studies, assessed the full text of potentially eligible studies against the inclusion criteria and carried out data extraction using customised forms (supplementary material, appendix 4). Disagreements were resolved through consultation between the two reviewers and discussion with other researchers if needed.

The methodological quality was assessed independently by two researchers using the Effective Public Health Practice Project (EPHPP) [20] for observational and the Cochrane Effective Practice and Organisation of Care (EPOC) criteria [21] for intervention studies.

For each publication, the method(s) used to quantify VOC exposure were assessed for the likelihood of providing a valid quantification of long-term individual domestic VOC exposure. This grading scheme is broadly based on the principle that longer averaging times are less susceptible to the influence of short-term peaks and troughs, and the evidence that area or static sampling can under- or over-estimate personal exposure (table 1) [22].

View this table:
  • View inline
  • View popup
TABLE 1

Hierarchy of volatile organic compound exposure measurement

Due to the substantial heterogeneity in populations, exposures and outcome measures, meta-analysis of the included studies was deemed inappropriate and was not conducted. A descriptive and narrative synthesis of the evidence was therefore undertaken. In interpreting the evidence we preferentially drew, wherever possible, on evidence from experimental studies and observational studies judged to be at low risk of bias.

Results

Description of studies

Our searches identified 8455 potentially relevant papers; 852 papers were removed after de-duplication, leaving 7603 unique papers that were subjected to screening. Of these, 53 satisfied our inclusion criteria (fig. 1).

FIGURE 1
  • Download figure
  • Open in new tab
  • Download powerpoint
FIGURE 1

Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) flow diagram of studies identified to investigate the role of domestic volatile organic compound (VOC) exposure in risk of developing and/or exacerbating asthma and allergic disorders. RCT: randomised controlled trial; CCT: controlled clinical trial; CBA: controlled before-and-after.

We found eight interventional studies: one RCT [23], one CCT [24] and six CBA studies [25–30]. The majority (n=45) of studies employed observational designs. There were six cohort studies [31–36] and 11 case–control studies [37–47]. Among the observational studies, two-thirds (n=28) were cross-sectional studies [48–75].

30 studies investigated the role of VOCs in the context of developing asthma/allergy [25, 28, 31, 36, 37, 40–46, 48–54, 57, 59, 61–65, 67–69, 73]; five studies investigated the role of VOCs in exacerbating established asthma/allergy [24, 27, 32, 33, 56]; and the remaining 18 studies investigated the role of VOCs in both the development and exacerbation of asthma/allergy [23, 26, 29, 30, 34, 35, 38, 39, 47, 55, 58, 60, 66, 70–72, 74, 75] (table S1).

Quality assessment

Five studies, including one RCT [23], three cohort studies [33–35] and one case–control study [47], were graded as being at low risk of bias; 15 studies, including two cohort studies [31, 36], five case–control studies [37, 42–45] and eight cross-sectional studies [48, 50, 62, 65, 72–75], were graded as being at moderate risk of bias. The remaining 33 studies were judged to be at high risk of bias (tables S1 and S1A).

Studies investigating the role of VOCs in the aetiology of asthma/allergy

Six studies examined the association between total VOCs and asthma/allergy-related outcomes [36, 43, 45, 46, 49, 51]. While one cohort study at moderate risk of bias found no associations [36], two case–control studies at moderate risk of bias reported adverse associations between total VOCs and asthma [43, 45]. There was one further study that measured total VOC exposure but did not relate this to the outcomes of interest [63].

Total VOCs were also investigated in one case–control study [46] and two cross-sectional studies [49, 51] that were considered to be at high risk of bias (tables S1A and S2).

Aromatic VOCs

14 studies explored the associations between the aromatic group of VOCs and asthma/allergy-related health outcomes (table S1A) [31, 37, 40–43, 45, 46, 50, 51, 54, 61, 62, 73]. Among the studies at moderate risk of bias, one cohort study reported a significant association between exposure to benzene and decreased CD4 CD25 regulatory T-cells in cord blood [31], two case–control studies [43, 45] and two cross-sectional studies [50, 62] reported adverse associations between aromatic VOCs and asthma, wheezing, nocturnal breathlessness and cord blood T-cell parameters, while two other case–control studies [37, 42] and one cross-sectional study [73] found no association between aromatics and asthma, atopic eczema/dermatitis, allergic rhino-conjunctivitis or sensitisation. Aromatic VOCs were measured in two other studies, but exposure was not related to any of the outcomes of interest [63, 69].

Aromatic VOCs were also investigated in three case–control studies [40, 41, 46] and three cross-sectional studies [51, 54, 61] that were all considered to be at high risk of bias.

Chlorinated hydrocarbons

Two cross-sectional studies at moderate risk of bias examined chlorinated hydrocarbons as a group, or chloroethenes separately, and reported adverse association with wheezing and cord blood T-cell parameters [50, 62]. These types of VOCs were also investigated in two cross-sectional studies that were judged to be at high risk of bias [51, 61].

Propylene glycol and glycol ethers

One case–control study at moderate risk of bias reported adverse associations between propylene glycol and glycol ethers and asthma, rhinitis, eczema and IgE-sensitisation [37]. Another cross-sectional study also investigated this exposure; however, this study was at high risk of bias (table S1A) [51].

Alkanes

Alkanes were investigated in six studies (table S1A) [37, 42, 43, 51, 61, 62]. Three case–control studies at moderate risk of bias reported no associations between alkanes and asthma, atopic dermatitis, allergic rhino-conjunctivitis, sensitisation or nocturnal breathlessness [37, 42, 43]. One cross-sectional study at moderate risk of bias found adverse associations between methylcyclopentane and elevated percentages of interleukin-4-producing type 2 T-cells [62]. The remaining two cross-sectional studies were at high risk of bias [51, 61].

Alcohols

Alcohols were investigated in three cross-sectional studies; all were considered to be at high risk of bias [49, 53, 59].

Aldehydes

Two studies, one case–control [37] and one cross-sectional [48], at moderate risk of bias, found no association between aldehydes as a class and the outcomes of interest (table S1A). Formaldehyde was the most commonly reported individual aldehyde (17 studies) [25, 36, 40–44, 46, 48, 49, 51, 54, 57, 64, 65, 67, 68]. Among six studies at moderate risk of bias, one case–control study showed no associations with asthma [42], while one cohort study [36], two case–control studies [43, 44] and two cross-sectional studies [48, 65] at moderate risk of bias found adverse associations between formaldehyde exposure and asthma, allergic rhinitis, rhino-conjunctivitis, atopic eczema or nocturnal breathlessness. Four studies measured formaldehyde but did not relate exposure to the outcomes of interest [28, 52, 63, 69]. 11 remaining studies [25, 40, 41, 46, 49, 51, 54, 57, 64, 67, 68] on formaldehyde exposure were at high risk of bias.

Acrolein was investigated in one cross-sectional study at moderate risk of bias and found to be adversely associated with the prevalence of asthma in the past year in those with atopic asthma but not with nonatopic asthma [48]. A second cross-sectional study also assessed acrolein exposure; however, this study was at high risk of bias [51].

Acetaldehyde was investigated in four studies; all were considered to be at high risk of bias (table S1A) [41, 51, 57, 64].

Ketones

Ketones were investigated in three studies; all were considered to be at high risk of bias (table S1A) [49, 53, 59].

Terpenes

Terpenes were investigated in two studies at moderate risk of bias [43, 62]. In a case–control study, exposure to limonene was related to bronchial hyperresponsiveness and exposure to α-pinene and carenes (δ2, δ3) to a reduction in peak expiratory flow [43], while a cross-sectional study failed to relate any of these exposures to allergic sensitisation to food allergens [62]. Terpenes were also investigated in one study that was at high risk of bias (table S1A) [61].

VOCs only investigated in single studies

In one cross-sectional study at moderate risk of bias, chloroform as a single compound was associated with wheezing, and methyl t-butyl ether was associated with physician-diagnosed asthma and wheezing [50]. One case–control study at moderate risk of bias also reported that total terpene exposure was linked to nocturnal breathlessness [43].

Two other case–control studies at moderate risk of bias reported no association between exposure to organic acids as a class and asthma, eczema, allergic rhinoconjunctivitis and sensitisation [37], or between butanols as a class and asthma, sensitisation and lung function [43]. VOCs were also investigated in five other single studies at high risk of bias (table S5) [49, 51–53, 59].

Summary

Overall, we found a substantial body of evidence, the majority of which was judged to be at high risk of bias. Whilst it was therefore not possible to draw any conclusive assessment in relation to the aetiological role of VOCs in the development of asthma/allergy, the modest effect sizes and the heterogeneity of findings suggest that VOC exposure is unlikely to be a major risk factor for the development of asthma/allergy in the general population.

Studies investigating the effects of VOCs in established asthma/allergy

Total VOCs were investigated but not examined in relation to the outcome, in two studies, both of which were considered to be at high risk of bias (tables S1A and S3) [24, 27].

Aromatic VOCs

Total aromatic VOCs were investigated in four studies [27, 32, 33, 56]. One cohort study at low risk of bias reported that exposure to benzene, toluene and ethylbenzene was associated with a decrease in forced expiratory volume in 1 s (FEV1) and with an increase in change of FEV1 [33]. Exposure to these aromatics also leads to an increase in rescue medication and emergency department visits. Two studies measured toluenes [27, 56], two studies measured xylenes [27, 56], and one study measured styrenes [32], but none of these examined these exposures in relation to the outcomes of interest. These studies were judged as being at high risk of bias [27, 32, 56].

Aldehydes

Formaldehyde was investigated in one cohort study at low risk of bias that found no association with asthma/allergic disease exacerbation [33]. Two other studies also measured aldehydes but did not examine exposure in relation to the outcome of interest, and these were furthermore considered to be at high risk of bias [24, 27].

Summary

Overall, we found a much smaller body of evidence focusing on investigating the relationship between VOC exposure and asthma/allergy exacerbations in those with established disease. This evidence was highly heterogeneous and therefore inconclusive.

Studies investigating the role of VOCs in both aetiology and established disease

Out of eight studies that measured total VOCs, five did not relate exposure to outcomes [26, 29, 35, 58, 72]. The one case–control study at low risk of bias that analysed exposure–outcome relationships found no association [47]; the remaining two studies that also investigated total VOCs were at high risk of bias (see table S1A) [55, 70].

Four studies measured aromatics [26, 58, 70, 71], two studies measured chlorinated VOCs [26, 58], three studies measured alkanes [58, 70, 72], two studies measured alcohols [35, 38], three studies measured aldehydes [35, 71, 72], two studies measured ketones [35, 38], one study measured terpenes [70] and one study measured esters [72], but they did not examine these VOCs in relation to the outcome of interest.

Aldehydes

Formaldehyde was investigated in 14 studies [23, 30, 34, 35, 39, 47, 58, 60, 66, 70–72, 74, 75]. One RCT with low risk of bias reported adverse associations between formaldehyde and wheezing [23]. One cohort study at low risk of bias found no associations between formaldehyde and wheezing [34]; in contrast, one case–control at low risk of bias [47] and two cross-sectional studies at moderate risk of bias [74, 75] showed positive associations between formaldehyde and current asthma severity, wheezing/severity and nocturnal breathlessness (table S1A).

Esters

Assessment of 2,2,4-trimethyl-1,3-pentanediol diisobutyrate was carried out in two cross-sectional studies. One of these, at moderate risk of bias, did not relate exposure to asthma/allergy-related outcomes [72], while the second study was at high risk of bias (table S1A) [71].

Summary

The key additional insight from this body of work focusing on both asthma/allergy incidence and risk of exacerbation is that there was one well-conducted RCT which found that exposure to low-VOC (formaldehyde)-emitting heating resulted in reduced respiratory symptoms in children with atopic disease, but this had no impact on lung function.

Unpublished and ongoing studies

No relevant unpublished and/or ongoing studies were identified.

Discussion

This systematic review is probably the most comprehensive investigation undertaken to date of the role of VOCs in the development of asthma/allergic disease and in exacerbating established asthma/allergy. Most studies investigated the possible role of VOCs in the development of asthma and/or allergic disease, with relatively few studies relating VOCs to exacerbations/severity of established disease. The overwhelming majority of studies employed observational designs, with aromatics and formaldehyde being the main VOCs studied. Critical appraisal of included studies suggested that there was a substantial risk of bias in this body of knowledge. There were approximately equal numbers of studies reporting either adverse associations of various VOCs or no association. Moreover, the numbers of studies supporting and not supporting the associations were also fairly balanced in terms of their methodological quality. In addition, only four of the included studies (one cohort [31], one case–control [42] and two cross-sectional [50, 65]) employed exposure assessment methodology that can be considered acceptable in generating the data for exposure–outcome analysis. Given the methodological concerns and the inconsistent results, these data do not provide sufficient evidence to unequivocally support or refute the hypothesis that domestic VOC exposure is associated with an increased risk of developing and/or exacerbating asthma/allergy.

A key strength of this systematic review is the comprehensiveness of the searches. We carefully identified all VOCs and then grouped and scrutinised them under several categories to find the effect of each compound on the development of asthma/allergy and exacerbating established disease. The methods used to quantify VOC exposure were carefully assessed and graded for methodological rigour. We note that the existing quality assessment tools do not incorporate assessment of the quality of the exposure information; consequently, studies rated as strong methodologically could have weak methods of quantifying personal VOC exposures. We believe this systematic review to have been more rigorous than the previous, frequently cited, systematic review [76], critical analysis [77] and literature review [78], which notably did not critically appraise study quality using validated tools or distinguish between studies investigating aetiology and those investigating established disease.

The main limitations of this review stem from the heterogeneity of populations, exposures and outcomes studied, and the overall limited body of high quality studies. The many limitations of the conducted studies include: inadequate sampling of VOCs at home or in schools; exposure assessment tending to be short-term (typically ≤24 h) and carried out by area sampling with very few personal sampling studies over extended periods; lack of standardisation in assessing asthma/allergy-related health outcomes; measurement of many VOCs that were not related to relevant health outcomes of interest; frequent inadequate adjustment for confounding factors; failure to adjust for clustering; failure to distinguish between disease aetiology, severity and treatment of established disease; and failure to adjust for or consider the consequence of multiple tests of statistical comparison. A potent source of indoor VOC exposure is environmental tobacco smoke, and a further limitation of our methodology was the deliberate exclusion of studies that had utilised VOC measurements as a proxy measure for environmental tobacco smoke exposure, because the focus of this study was residential VOC exposure from noncigarette sources. Notably, some studies failed to adjust for the smoking habits of household members.

Animal studies demonstrate that VOC exposure can influence the immune responses, increasing T-helper cell (Th) type 2 polarisation [79–81]. In humans, increased Th2 polarisation of neonatal immune responses has been associated with maternal VOC exposure during pregnancy [82]. Although little evidence exists suggesting that VOCs influence lung growth, embryotoxic effects from exposure to airborne VOCs on murine embryonic stem cells have been reported [83], and adverse effects on rat embryo/fetal development have been linked to VOC release from their cages [84].

Asthma and allergic diseases are a significant burden to the health services of industrialised countries and a potential threat to the health services of developing countries. The identification of environmental exposures that increase the risk of developing these conditions or exacerbating established disease is warranted. Whether VOCs have adverse effects on asthma/allergy is important to ascertain, given that intervention to reduce VOC exposure is feasible by lifestyle changes (e.g. avoiding redecoration, air fresheners and perfumed items; having a smoke-free home; increasing ventilation) and technological adaptation (e.g. use of low-emitting VOC materials). Despite the aforementioned shortcomings in the underpinning evidence base and the inconsistent findings, this work has demonstrated that it is not yet possible to exclude the possibility that VOCs, particularly aromatics, aldehydes (formaldehyde), alkanes and terpenes, may play a harmful role in the development of asthma/allergy and/or in exacerbating established disease.

Further work is required to clarify the impact of VOCs on the development/exacerbation of asthma/allergy. In the first instance, there is a need for well-designed, large cohort studies relating long-term, indoor, personal exposure measurements to validated asthma/allergy-related health outcomes with adequate adjustment for key potential confounding factors and effect modifiers. These observational studies may then need to be followed by well-conducted RCTs investigating the effectiveness and cost-effectiveness of interventions reducing VOC exposure on the risk of developing asthma/allergy and/or exacerbating established disease.

Conclusion

The overall body of evidence in relation to the role of VOCs in the development of asthma and allergic disease and the role of VOCs in exacerbating established asthma/allergy in children and adults is weak. We found very few interventional studies and data were generally of poor quality, being derived mainly from observational studies. There is a need to develop a more definitive evidence base to examine the relationship between VOC exposure and asthma/allergy, in order to inform deliberations on public policy and clinical care.

Acknowledgements

We would like to thank Marshall Dozier (The University of Edinburgh, Edinburgh, UK) for her advice on the literature searches. We acknowledge the contribution of an international panel of experts and thank them for providing information on unpublished/ongoing studies. Our thanks also go to Anna Wierzoch (The University of Edinburgh) for administrative support.

Footnotes

  • This article has supplementary material available from err.ersjournals.com

  • Support statement: This work was funded in its entirety by a project grant awarded by the Chief Scientist's Office of the Scottish Government Health Dept (CZG/2/573). The funding source had no role in the study design, data collection, analysis, and interpretation, in preparation of the manuscript, or the decision to submit it for publication.

  • Conflict of interest: Disclosures can be found alongside the online version of this article at err.ersjournals.com

  • Provenance: Submitted article, peer reviewed.

  • Received January 21, 2014.
  • Accepted April 27, 2014.
  • Copyright ©ERS 2015.

ERR articles are open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.

References

  1. ↵
    1. Barnett SBL,
    2. Nurmagambetov TA.
    Costs of asthma in the United States: 2002–2007. J Allergy Clin Immunol 2011; 127: 145–152.
    OpenUrlCrossRefPubMed
  2. ↵
    1. Patel DA,
    2. Holdford DA,
    3. Edwards E, et al.
    Estimating the economic burden of food-induced allergic reactions and anaphylaxis in the United States. J Allergy Clin Immunol 2011; 128: 110–115.
    OpenUrlCrossRefPubMed
  3. ↵
    1. Simpson CR,
    2. Sheikh A.
    Trends in the epidemiology of asthma in England: a national study of 333 294 patients. J R Soc Med 2010; 103: 98–106.
    OpenUrlAbstract/FREE Full Text
    1. Simpson CR,
    2. Newton J,
    3. Hippisley-Cox J, et al.
    Incidence and prevalence of multiple allergic disorders recorded in a national primary care database. J R Soc Med 2008; 101: 558–563.
    OpenUrlAbstract/FREE Full Text
    1. Ghouri N,
    2. Hippisley-Cox J,
    3. Newton J, et al.
    Trends in the epidemiology and prescribing of medication for allergic rhinitis in England. J R Soc Med 2008; 101: 466–472.
    OpenUrlAbstract/FREE Full Text
    1. Gupta R,
    2. Sheikh A,
    3. Strachan DP, et al.
    The trends in allergic disorders in the UK. Thorax 2007; 62: 91–96.
    OpenUrlAbstract/FREE Full Text
    1. Jenner N,
    2. Campbell J,
    3. Marks R.
    Morbidity and cost of atopic eczema in Australia. Australas J Dermatol 2004; 45: 16–22.
    OpenUrlCrossRefPubMed
    1. Ninan TK,
    2. Russell G.
    Respiratory symptoms and atopy in Aberdeen schoolchildren: evidence from two surveys 25 years apart. BMJ 1992; 304: 873–875.
    OpenUrlAbstract/FREE Full Text
    1. Omran M,
    2. Russell G.
    Continuing increase in respiratory symptoms and atopy in Aberdeen schoolchildren. BMJ 1996; 312: 34.
    OpenUrlFREE Full Text
    1. Devenny A,
    2. Wassall H,
    3. Ninan T, et al.
    Respiratory symptoms and atopy in children in Aberdeen: questionnaire studies of a defined school population repeated over 35 years. BMJ 2004; 329: 489–490.
    OpenUrlFREE Full Text
    1. Tagiyeva N,
    2. McNeill G,
    3. Russell G, et al.
    Two main subtypes of wheezing illness? Evidence from the 2004 Aberdeen schools asthma survey. Pediatr Allergy Immunol 2008; 19: 7–12.
    OpenUrlPubMed
  4. ↵
    1. Mannino DM,
    2. Homa DM,
    3. Akinbami LJ, et al.
    Surveillance for asthma – United States, 1980–1999. MMWR Surveill Summ 2002; 51: 1–13.
    OpenUrlPubMed
  5. ↵
    United States Environmental Protection Agency. An Introduction to Indoor Air Quality (IAQ). Volatile Organic Compounds (VOCs). www.epa.gov/iaq/voc.html Date last updated: July 9, 2012.
  6. ↵
    1. Franklin PJ.
    Indoor air quality and respiratory health of children. Paediatr Respir Rev 2007; 8: 281–286.
    OpenUrlCrossRefPubMed
  7. ↵
    1. Zhang J,
    2. Smith KR.
    Indoor air pollution: a global health concern. Br Med Bull 2003; 68: 209–225.
    OpenUrlAbstract/FREE Full Text
  8. ↵
    1. Dales R,
    2. Raizenne M.
    Residential exposure to volatile organic compounds and asthma. J Asthma 2004; 41: 259–270.
    OpenUrlCrossRefPubMed
  9. ↵
    1. Farrow A,
    2. Taylor H,
    3. Golding J.
    Time spent in the home by different family members. Environ Technol 1997; 8: 605–614.
    OpenUrl
  10. ↵
    1. Sherriff A,
    2. Farrow A,
    3. Golding J, et al.
    Frequent use of chemical household products is associated with persistent wheezing in pre-school age children. Thorax 2005; 60: 45–49.
    OpenUrlAbstract/FREE Full Text
  11. ↵
    1. Herbarth O,
    2. Fritz GJ,
    3. Rehwagen M, et al.
    Association between indoor renovation activities and eczema in early childhood. Int J Hyg Environ Health 2006; 209: 241–247.
    OpenUrlCrossRefPubMed
  12. ↵
    Effective Public Health Practice Project (EPHPP). Quality assessment tool for quantitative studies. www.ephpp.ca/tools.html Date last accessed: December 13, 2012.
  13. ↵
    Cochrane Effective Practice and Organisation of Care (EPOC) Review Group. Data Collection Checklist. Ottawa, EPOC, 2002. Available from http://epoc.cochrane.org/sites/epoc.cochrane.org/files/uploads/datacollectionchecklist.pdf
  14. ↵
    1. Harrison RM,
    2. Thornton CA,
    3. Lawrence RG, et al.
    Personal exposure monitoring of particular matter, nitrogen dioxide, and carbon monoxide, including susceptible groups. Occup Environ Med 2002; 59: 671–679.
    OpenUrlAbstract/FREE Full Text
  15. ↵
    1. Marks GB,
    2. Ezz W,
    3. Aust N, et al.
    Respiratory health effects of exposure to low-NOx unflued gas heaters in the classroom: a double-blind, cluster-randomized, crossover study. Environ Health Perspect 2010; 118: 1476–1482.
    OpenUrlCrossRefPubMed
  16. ↵
    1. Tuomainen M,
    2. Tuomainen A,
    3. Liesivuori J, et al.
    The 3-year follow-up study in a block of flats – experiences in the use of the Finnish indoor climate classification. Indoor Air 2003; 13: 136–147.
    OpenUrlCrossRefPubMed
  17. ↵
    1. Broder I,
    2. Corey P,
    3. Cole P, et al.
    Comparison of health of occupants and characteristics of houses among control homes and homes insulated with urea formaldehyde foam. II. Initial health and house variables and exposure–response relationships. Environ Res 1988; 45: 156–178.
    OpenUrlPubMed
  18. ↵
    1. Brugge D,
    2. Vallarino J,
    3. Ascolillo L, et al.
    Comparison of multiple environmental factors for asthmatic children in public housing. Indoor Air 2003; 13: 18–27.
    OpenUrlCrossRefPubMed
  19. ↵
    1. Kim JH,
    2. Lee KM,
    3. Koh SB, et al.
    Effect of polyurushiol paint on indoor air quality and atopic dermatitis. Korean J Dermatol 2010; 48: 198–205.
    OpenUrl
  20. ↵
    1. Norbäck D,
    2. Wieslander G,
    3. Zhang X, et al.
    Respiratory symptoms, perceived air quality and physiological signs in elementary school pupils in relation to displacement and mixing ventilation system: an intervention study. Indoor Air 2011; 21: 427–437.
    OpenUrlCrossRefPubMed
  21. ↵
    1. Putus T,
    2. Tuomainen A,
    3. Rautiala S.
    Chemical and microbial exposures in a school building: adverse health effects in children. Arch Environ Health 2004; 59: 194–201.
    OpenUrlCrossRefPubMed
  22. ↵
    1. Wantke F,
    2. Demmer CM,
    3. Tappler P, et al.
    Exposure to gaseous formaldehyde induces IgE-mediated sensitization to formaldehyde in school-children. Clin Exp Allergy 1996; 26: 276–280.
    OpenUrlCrossRefPubMed
  23. ↵
    1. Baïz N,
    2. Slama R,
    3. Béné MC, et al.
    Maternal exposure to air pollution before and during pregnancy related to changes in newborn’s cord blood lymphocyte subpopulations. The EDEN study cohort. BMC Pregnancy Childbirth 2011; 11: 87.
    OpenUrlCrossRefPubMed
  24. ↵
    1. Diez U,
    2. Kroessner T,
    3. Rehwagen M, et al.
    Effects of indoor painting and smoking on airway symptoms in atopy risk children in the first year of life results of the LARS-study. Leipzig Allergy High-Risk Children Study. Int J Hyg Environ Health 2000; 203: 23–28.
    OpenUrlCrossRefPubMed
  25. ↵
    1. Martins PC,
    2. Valente J,
    3. Papoila AL, et al.
    Airways changes related to air pollution exposure in wheezing children. Eur Respir J 2012; 39: 246–253.
    OpenUrlAbstract/FREE Full Text
  26. ↵
    1. Raaschou-Nielsen O,
    2. Hermansen MN,
    3. Loland L, et al.
    Long-term exposure to indoor air pollution and wheezing symptoms in infants. Indoor Air 2010; 20: 159–167.
    OpenUrlCrossRefPubMed
  27. ↵
    1. Smedje G,
    2. Norbäck D.
    New ventilation systems at select schools in Sweden – effects on asthma and exposure. Arch Environ Health 2000; 55: 18–25.
    OpenUrlCrossRefPubMed
  28. ↵
    1. Smedje G,
    2. Norbäck D.
    Incidence of asthma diagnosis and self-reported allergy in relation to the school environment – a four-year follow-up study in schoolchildren. Int J Tuberc Lung Dis 2001; 5: 1059–1066.
    OpenUrlPubMed
  29. ↵
    1. Choi H,
    2. Schmidbauer N,
    3. Sundell J, et al.
    Common household chemicals and the allergy risks in pre-school age children. PLoS One 2010; 5: e13423.
    OpenUrlCrossRefPubMed
  30. ↵
    1. Dewey S,
    2. Sagunski H,
    3. Palmgren U, et al.
    Mikrobielle flüchtige organische Verbindungen in der Raumluft: Ein neuer diagnostischer Ansatz bei feuchten und verschimmelten Wohnräumen? [Microbial volatile organic compounds: a new approach in assessing health risks by indoor mould?] Zbl Hyg 1995; 197: 504–515.
    OpenUrl
  31. ↵
    1. Garrett MH,
    2. Hooper MA,
    3. Hooper BM, et al.
    Increased risk of allergy in children due to formaldehyde exposure in homes. Allergy 1999; 54: 330–337.
    OpenUrlCrossRefPubMed
  32. ↵
    1. Gee IL,
    2. Watson AFR,
    3. Tavernier G, et al.
    Indoor air quality, environmental tobacco smoke and asthma: a case control study of asthma in a community population. Indoor Built Environ 2005; 14: 215–219.
    OpenUrlCrossRef
  33. ↵
    1. Hulin M,
    2. Caillaud D,
    3. Annesi-Maesano I.
    Indoor air pollution and childhood asthma: variations between urban and rural areas. Indoor Air 2010; 20: 502–514.
    OpenUrlCrossRefPubMed
  34. ↵
    1. Hwang G,
    2. Yoon C,
    3. Choi J.
    A case–control study: exposure assessment of VOCs and formaldehyde for asthma in children. Aerosol Air Qual Res 2011; 11: 908–914.
    OpenUrl
  35. ↵
    1. Norbäck D,
    2. Björnsson E,
    3. Janson C, et al.
    Asthmatic symptoms and volatile organic compounds, formaldehyde, and carbon dioxide in dwellings. Occup Environ Med 1995; 52: 388–395.
    OpenUrlAbstract/FREE Full Text
  36. ↵
    1. Rumchev KB,
    2. Spickett JT,
    3. Bulsara MK, et al.
    Domestic exposure to formaldehyde significantly increases the risk of asthma in young children. Eur Respir J 2002; 20: 403–408.
    OpenUrlAbstract/FREE Full Text
  37. ↵
    1. Rumchev K,
    2. Spickett J,
    3. Bulsara M, et al.
    Association of domestic exposure to volatile organic compounds with asthma in young children. Thorax 2004; 59: 746–751.
    OpenUrlAbstract/FREE Full Text
  38. ↵
    1. Tavernier G,
    2. Fletcher G,
    3. Gee I, et al.
    IPEADAM study: indoor endotoxin exposure, family status, and some housing characteristics in English children. J Allergy Clin Immunol 2006; 117: 656–662.
    OpenUrlCrossRefPubMed
  39. ↵
    1. Venn AJ,
    2. Cooper M,
    3. Antoniak M, et al.
    Effects of volatile organic compounds, damp, and other environmental exposures in the home on wheezing illness in children. Thorax 2003; 58: 955–960.
    OpenUrlAbstract/FREE Full Text
  40. ↵
    1. Annesi-Maesano I,
    2. Hulin M,
    3. Lavaud F, et al.
    Poor air quality in classrooms related to asthma and rhinitis in primary schoolchildren of the French 6 Cities Study. Thorax 2012; 67: 682–688.
    OpenUrlAbstract/FREE Full Text
  41. ↵
    1. Araki A,
    2. Kanazawa A,
    3. Kawai T, et al.
    The relationship between exposure to microbial volatile organic compound and allergy prevalence in single-family homes. Sci Total Environ 2012; 423: 18–26.
    OpenUrlCrossRefPubMed
  42. ↵
    1. Arif AA,
    2. Shah SM.
    Association between personal exposure to volatile organic compounds and asthma among US adult population. Int Arch Occup Environ Health 2007; 80: 711–719.
    OpenUrlCrossRefPubMed
  43. ↵
    1. Billionnet C,
    2. Gay E,
    3. Kirchner S, et al.
    Quantitative assessments of indoor air pollution and respiratory health in a population-based sample of French dwellings. Environ Res 2011; 111: 425–434.
    OpenUrlPubMed
  44. ↵
    1. Chubirko MI,
    2. Stepkin YI,
    3. Pichuzhkina NM, et al.
    [Risk factors of the intra-housing environment to human health.] Gig Sanit 2005; 1: 11–12.
    OpenUrlPubMed
  45. ↵
    1. Elke K,
    2. Begerow J,
    3. Oppermann H, et al.
    Determination of selected microbial volatile organic compounds by diffusive sampling and dual-column capillary GC-FID – a new feasible approach for the detection of an exposure to indoor mould fungi? J Environ Monit 1999; 1: 445–452.
    OpenUrlCrossRefPubMed
  46. ↵
    1. Erdei E,
    2. Bobvos J,
    3. Brozik M, et al.
    Indoor air pollutants and immune biomarkers among Hungarian asthmatic children. Arch Environ Health 2003; 58: 337–347.
    OpenUrlPubMed
  47. ↵
    1. Fraga S,
    2. Ramos E,
    3. Martins A, et al.
    Indoor air quality and respiratory symptoms in Porto schools. Rev Port Pneumol 2008; 14: 487–507.
    OpenUrlPubMed
  48. ↵
    1. Gordian ME,
    2. Stewart AW,
    3. Morris SS.
    Evaporative gasoline emissions and asthma symptoms. Int J Environ Res Public Health 2010; 7: 3051–3062.
    OpenUrlCrossRefPubMed
  49. ↵
    1. Hulin M,
    2. Annesi-Maesano I,
    3. Caillaud D.
    Qualité de l'air intérieur dans les écoles et asthme et allergies parmi les écoliers en Auvergne. Différences entre le milieu rural et le milieu urbain. [Indoor air quality at school and allergy and asthma among schoolchildren. Differences between rural and urban areas.] Revue Francaise d'Allergologie 2011; 51: 419–424.
    OpenUrlCrossRef
  50. ↵
    1. Khalequzzaman M,
    2. Kamijima M,
    3. Sakai K, et al.
    Indoor air pollution and its impact on children under five years old in Bangladesh. Indoor Air 2007; 17: 297–304.
    OpenUrlCrossRefPubMed
  51. ↵
    1. Kim JL,
    2. Elfman L,
    3. Mi Y, et al.
    Indoor molds, bacteria, microbial volatile organic compounds and plasticizers in schools – associations with asthma and respiratory symptoms in pupils. Indoor Air 2007; 17: 153–163.
    OpenUrlCrossRefPubMed
  52. ↵
    1. Krzyzanowski M,
    2. Quackenboss JJ,
    3. Lebowitz MD.
    Chronic respiratory effects of indoor formaldehyde exposure. Environ Res 1990; 52: 117–125.
    OpenUrlCrossRefPubMed
  53. ↵
    1. Lehmann I,
    2. Rehwagen M,
    3. Diez U, et al.
    Enhanced in vivo IgE production and T cell polarization toward the type 2 phenotype in association with indoor exposure to VOC: results of the LARS study. Int J Hyg Environ Health 2001; 204: 211–221.
    OpenUrlCrossRefPubMed
  54. ↵
    1. Lehmann I,
    2. Thoelke A,
    3. Rehwagen M, et al.
    The influence of maternal exposure to volatile organic compounds on the cytokine secretion profile of neonatal T cells. Environ Toxicol 2002; 17: 203–210.
    OpenUrlCrossRefPubMed
  55. ↵
    1. Liu FY,
    2. Sun Z,
    3. Xiao YY.
    Influence of indoor decoration pollution on children’s health. J Environ Health 2010; 27: 1077–1079.
    OpenUrl
  56. ↵
    1. Lovreglio P,
    2. Carrus A,
    3. Iavicoli S, et al.
    Indoor formaldehyde and acetaldehyde levels in the province of Bari, South Italy, and estimated health risk. J Environ Monit 2009; 11: 955–961.
    OpenUrlCrossRefPubMed
  57. ↵
    1. Matsunaga I,
    2. Miyake Y,
    3. Yoshida T, et al.
    Ambient formaldehyde levels and allergic disorders among Japanese pregnant women: baseline data from the Osaka maternal and child health study. Ann Epidemiol 2008; 18: 78–84.
    OpenUrlCrossRefPubMed
  58. ↵
    1. Mi YH,
    2. Norbäck D,
    3. Tao J, et al.
    Current asthma and respiratory symptoms among pupils in Shanghai, China: influence of building ventilation, nitrogen dioxide, ozone, and formaldehyde in classrooms. Indoor Air 2006; 16: 454–464.
    OpenUrlCrossRefPubMed
  59. ↵
    1. Norbäck D,
    2. Walinder R,
    3. Wieslander G, et al.
    Indoor air pollutants in schools: nasal patency and biomarkers in nasal lavage. Allergy 2000; 55: 163–170.
    OpenUrlCrossRefPubMed
  60. ↵
    1. Palczynski C,
    2. Krakowiak A,
    3. Hanke W, et al.
    Indoor formaldehyde exposure and airway allergic diseases. Int Rev Allergol Clin Immunol 1999; 5: 65–69.
    OpenUrl
  61. ↵
    1. Rudnai P,
    2. Viragh Z,
    3. Vaskovi EB, et al.
    Egyes lakoteri tenyezok szerepe iskolas gyermekek legzoszervi panaszainak es allergias tuneteinek gyakorisagaban. [Role of some indoor factors in the prevalence of respiratory symptoms and allergy among school-children in six towns of Hungary.] Egeszsegtudomany 1999; 43: 196–208.
    OpenUrl
  62. ↵
    1. Smedje G,
    2. Norbäck D,
    3. Edling C.
    Asthma among secondary schoolchildren in relation to the school environment. Clin Exp Allergy 1997; 27: 1270–1278.
    OpenUrlCrossRefPubMed
  63. ↵
    1. Villberg K,
    2. Mussalo-Rauhamaa H,
    3. Haahtela T, et al.
    Prevalence of plastic additives in indoor air related to newly diagnosed asthma. Indoor Built Environ 2008; 17: 455–459.
    OpenUrlCrossRef
  64. ↵
    1. Wieslander G,
    2. Norbäck D,
    3. Björnsson E, et al.
    Asthma and the indoor environment: the significance of emission of formaldehyde and volatile organic compounds from newly painted indoor surfaces. Int Arch Occup Environ Health 1997; 69: 115–124.
    OpenUrlCrossRefPubMed
  65. ↵
    1. Wu JG,
    2. Tang CX,
    3. Zhuang ZJ, et al.
    Effect of indoor air pollution related to traffic and fuel gas using for cooking on respiratory diseases in children and teenagers in urban area of Shanghai. J Environ Health 2010; 27: 244–247.
    OpenUrl
  66. ↵
    1. Yeatts KB,
    2. El-Sadig M,
    3. Leith D, et al.
    Indoor air pollutants and health in the United Arab Emirates. Environ Health Perspect 2012; 120: 687–694.
    OpenUrlCrossRefPubMed
  67. ↵
    1. Zhao Z,
    2. Sebastian A,
    3. Larsson L, et al.
    Asthmatic symptoms among pupils in relation to microbial dust exposure in schools in Taiyuan, China. Pediatr Allergy Immunol 2008; 19: 455–465.
    OpenUrlCrossRefPubMed
  68. ↵
    1. Fuentes-Leonarte V,
    2. Tenias JM,
    3. Ballester F.
    Levels of pollutants in indoor air and respiratory health in preschool children: a systematic review. Pediatr Pulmonol 2009; 44: 231–243.
    OpenUrlCrossRefPubMed
  69. ↵
    1. Dales R,
    2. Raizenne M.
    Residential exposure to volatile organic compounds and asthma. J Asthma 2004; 41: 259–270.
    OpenUrlCrossRefPubMed
  70. ↵
    1. Kim KH,
    2. Jahan SA,
    3. Kabir E.
    A review on human health perspective of air pollution with respect to allergies and asthma. Environ Int 2013; 59: 41–52.
    OpenUrlCrossRefPubMed
  71. ↵
    1. Bechtel DG,
    2. Waldner CL,
    3. Wickstrom M.
    Associations between in utero exposure to airborne emissions from oil and gas production and processing facilities and immune system outcomes in neonatal beef calves. Arch Environ Occup Health 2009; 64: 59–71.
    OpenUrlCrossRefPubMed
    1. Shwe TTW,
    2. Yamamoto S,
    3. Nakajima D, et al.
    Modulation of neurological related allergic reaction in mice exposed to low-level toluene. Toxicol Appl Pharmacol 2007; 222: 17–24.
    OpenUrlCrossRefPubMed
  72. ↵
    1. Fujimaki H,
    2. Yamamoto S,
    3. Shwe TTW, et al.
    Effect of long-term exposure to low-level toluene on airway inflammatory response in mice. Toxicol Lett 2007; 168: 132–139.
    OpenUrlCrossRefPubMed
  73. ↵
    1. Lehmann I,
    2. Thoelke A,
    3. Rehwagen M, et al.
    The influence of maternal exposure to volatile organic compounds on the cytokine secretion profile of neonatal T cells. Environ Toxicol 2002; 17: 203–210.
    OpenUrlCrossRefPubMed
  74. ↵
    1. Shen S,
    2. Yuan L,
    3. Zeng S.
    An effort to test the embryotoxicity of benzene, toluene, xylene, and formaldehyde to murine embryonic stem cells using airborne exposure technique. Inhal Toxicol 2009; 21: 973–978.
    OpenUrlCrossRefPubMed
  75. ↵
    1. Lee JC,
    2. Ahn TH,
    3. Yang YS, et al.
    Evaluation of embryo-fetal development in rats housed in concrete or hwangto cages during pregnancy. Birth Defects Res B Dev Reprod Toxicol 2008; 83: 32–39.
    OpenUrlCrossRefPubMed
View Abstract
PreviousNext
Back to top
View this article with LENS
Vol 24 Issue 135 Table of Contents
  • Table of Contents
  • Table of Contents (PDF)
  • Index by author
Email

Thank you for your interest in spreading the word on European Respiratory Society .

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Volatile organic compounds and risk of asthma and allergy: a systematic review
(Your Name) has sent you a message from European Respiratory Society
(Your Name) thought you would like to see the European Respiratory Society web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
Citation Tools
Volatile organic compounds and risk of asthma and allergy: a systematic review
Ulugbek B. Nurmatov, Nara Tagiyeva, Sean Semple, Graham Devereux, Aziz Sheikh
European Respiratory Review Mar 2015, 24 (135) 92-101; DOI: 10.1183/09059180.00000714

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero

Share
Volatile organic compounds and risk of asthma and allergy: a systematic review
Ulugbek B. Nurmatov, Nara Tagiyeva, Sean Semple, Graham Devereux, Aziz Sheikh
European Respiratory Review Mar 2015, 24 (135) 92-101; DOI: 10.1183/09059180.00000714
del.icio.us logo Digg logo Reddit logo Technorati logo Twitter logo CiteULike logo Connotea logo Facebook logo Google logo Mendeley logo
Full Text (PDF)

Jump To

  • Article
    • Abstract
    • Abstract
    • Introduction
    • Methods
    • Results
    • Discussion
    • Acknowledgements
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • PDF

Subjects

  • Asthma and allergy
  • Epidemiology, occupational and environmental lung disease
  • Tweet Widget
  • Facebook Like
  • Google Plus One

More in this TOC Section

  • Mucolytics for acute exacerbations of COPD: a meta-analysis
  • Targeting IL-33 and TSLP pathways for novel pulmonary therapeutics
  • Physical activity promotion interventions in chronic airways disease
Show more Reviews

Related Articles

Navigate

  • Home
  • Current issue
  • Archive

About the ERR

  • Journal information
  • Editorial board
  • Reviewers
  • Press
  • Permissions and reprints
  • Advertising
  • Sponsorship

The European Respiratory Society

  • Society home
  • myERS
  • Privacy policy
  • Accessibility

ERS publications

  • European Respiratory Journal
  • ERJ Open Research
  • European Respiratory Review
  • Breathe
  • ERS books online
  • ERS Bookshop

Help

  • Feedback

For authors

  • Instructions for authors
  • Publication ethics and malpractice
  • Submit a manuscript

For readers

  • Alerts
  • Subjects
  • RSS

Subscriptions

  • Accessing the ERS publications

Contact us

European Respiratory Society
442 Glossop Road
Sheffield S10 2PX
United Kingdom
Tel: +44 114 2672860
Email: journals@ersnet.org

ISSN

Print ISSN: 0905-9180
Online ISSN: 1600-0617

Copyright © 2023 by the European Respiratory Society