We thank Drs Kränke and Aberer for their interest in our study. Passive smoking is highly unlikely to have confounded the results. It is true that smoking is an indoor source of formaldehyde, although not a significant one in our study. Presence of fibreboard, particleboard flooring, house age, and indoor temperatures were the only significant predictors of formaldehyde levels. As shown by our original paper ( 1), which was cited, it would be almost impossible for tobacco smoking to have caused the associations seen between formaldehyde levels and atopy. Kränke and Aberer themselves note that passive smoking is not associated with the outcomes of interest; i.e., atopy and asthma. To be a confounder, a factor must not only be associated with the exposure, but must also cause the outcome in its own right.

The relevance of occupational exposure to formaldehyde is questionable. We would concede that it is probably not a major cause of occupational asthma. However, the epidemiologic studies that have been conducted in adults are biased by the well-known “healthy worker” effect. The occupational exposure limit of 300 ppb applies to the time-weighted average over an 8-h shift. The duration of sampling in our study was 4 days. Paustenbach et al. ( 2) actually recommended that an indoor level below (not above) 100 ppb should prevent irritation. Levels above 100 ppb were in fact detected in some homes.

However, it is also quite possible that formaldehyde does cause sensitization to common aeroallergens by some mechanism not involving respiratory irritation. For example, many formaldehyde compounds are well-recognized skin sensitizers ( 3). Furthermore, one probably does not need to be aware of respiratory irritation for the combination of aeroallergens and formaldehyde to have an effect on the immune system. This may be particularly relevant in children whose immune systems are still developing.

Of course, the speculation that formaldehyde may increase the risk of allergic sensitization in children remains unproven. Our paper aimed to suggest that this could be the case. We contend that this hypothesis is supported by our observations and those of Wantke et al. ( 4) in children and Wieslander et al. ( 5) in young adults. In summary, we agree that our data do not conclusively prove that an increased risk of atopic disease in children is due to low-level indoor formaldehyde exposure. However, we do believe that our data raise a hypothesis that may have been overlooked and that should be further tested before being dismissed as false.


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  2. References
  • 1
    Garrett MH, Hooper MA, Hooper BM. Formaldehyde in Australian homes – levels and sources. Clean Air – Australia 1997;31:28 32.
  • 2
    Paustenbach D, Alarie Y, Kulle T, et al. A recommended occupational exposure limit for formaldehyde based on irritation. J Toxicol Environ Health 1997;50:217 263.
  • 3
    Agner T, Flyvholm MA, Menne T. Formaldehyde allergy: a follow-up study. Am J Contact Dermatitis 1999;10:12 17.
  • 4
    Wantke F, Demmer CM, Tappler P, Götz M, Jarisch R. Exposure to gaseous formaldehyde induces IgE-mediated sensitisation to formaldehyde in schoolchildren. Clin Exp Allergy 1996;26:276 280.
  • 5
    Wieslander G, Norback D, Bjornsson E, Janson C, Boman G. 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.