The Importance of Preventing Dermal Exposure
Isocyanates have long been recognized as a primary cause of occupational asthma. Although exact figures as to the incidence of isocyanate hypersensitivity are difficult to assess, historical reviews estimate 3 to 5% of the workforce may develop asthma.1
Significant progress has been achieved in reducing isocyanate airborne exposures. The introduction of low vapor pressure isocyanates, such as MDI and pre-polymer formulations, have contributed to this success.
Of concern is the apparent failure of these efforts to reduce the incidence of isocyanate related asthma.2 MDI is now the main cause of this disorder.3 In some industries, MDI hypersensitivity exceeds historical incidence of asthma by 2 to 3 times.4
An article discussing "the role of the skin in development of chemical respiratory hypersensitivity"5 suggested that dermal exposures may be more effective than inhalation in inducing respiratory asthma.
Recent studies have confirmed the inability to sensitize animals via inhalation exposure to TDI and MDI.6, 7 In both studies, cutaneous (skin) contact induced respiratory sensitization in the majority of the animals. Another study concluded that the initial exposure to MDI via skin contact "may have profound effects upon the development of occupational asthma".8
This research suggests that preventing skin contact with isocyanates may be of primary importance in preventing isocyanate sensitization. In the :"Investigation of dermally induced airway hyperreactivity to toluene diisocyanate in guinea pigs", Bickis concluded that "the TLV should be assigned a skin notation (emphasis added) and appropriate warnings issued to all users."
1 Steven P. Levine, Ph.D., David H. Garabrant, M.D., A Critical Review of the Methods of Exposure Assessment and the Pulmonary Effects of TDI and MDI in Epidemiologic Studies, Final Report to the Chemical Manufacturers Association, November 10, 1994.
2 NIOSH Hazard Alert, Preventing Asthma and Death from Diisocyanate Exposure, March 1996
3 Bauer, Xavier, Hypersensitivity pneumonitis (extrinsic allergic alveolitis) induced by isocyanates. J. Allergy Clin Immunol, Vol. 95, Number 5, Part 1, May 1995
4 NIOSH Truss Joist MacMillan, HETA 93-0436, Deerwood, Minnesota, March 1996
5 Kimber, Ian, The role of the skin in the development of chemical respiratory hypersensitivity. Toxicology Letters 86(1996) 89-92, Elsevier Sciences B.V.
6 N.J. Rattray, P.A. Botham, P.M. Hext, D.R. Woodstock, I. Fielding, R.J. Dearman, I. Kimber, Induction of respiratory hypersensitivity to diphenylmethane-4-4'-diisocyanate (MDI) in guinea pigs. Influence route of exposure. Toxicology 88(1994) 15-30. Elsevier Science Ireland.
7 Ugis Bickis: Investigation of dermally induced airway hyperreactivity to toluene diisocyanate in guinea pigs. Ph.D. Thesis, Department of Pharmacology and Toxicology, Queen's University, Kingston, Canada November, 1994
8 R.J. Dearman, P.A. Botham, Inhalation Exposure to Respiratory Sensitizing Chemical - Down Regulates Pig lgE and Pulmonary Responses, Int Arch Allergy Appl Immunol 1990 92:245-432