Occupational respiratory hypersensitivity caused by preparations containing acrylates in dental personnel

Abstract

The results indicate that acrylates constitute an important hazard for dental workers. The mechanism of respiratory hypersensitivity is still unknown, and it is probably not IgE-mediated.

Workplace air quality and lung function among dental laboratory technicians

“…The potential occupational risk factors include chemical, physical, psychological, ergonomic, and other job-related factors Jacobsen, 1990, 1991;Jacobsen and Pettersen, 1993;Jacobsen et al, 1996;Wiltshire et al, 1996]. The health effects of concern include: potential adverse respiratory effects from inhalation of dusts from grinding and polishing of metal alloys, resins, ceramics, plaster, and the abrasives used for polishing [Choudat, 1994;Parks et al, 1999;Kelleher et al, 2000] or acrylates [Savonius et al, 1993;Piirilä et al, 1998;Nayebzadeh et al, 2000]; dermatitis from contact with acrylates and metals [Lee et al, 2001]; neurotoxicity [Seppäläinen and Rajaniemi, 1984] or disturbance of olfaction [Braun et al, 2002] by methyl methacrylate (MMA) monomer; genotoxic damage in lymphocytes possibly related to occupational exposure to chromium, cobalt, and nickel [Burgaz et al, 2002], and health complaints caused by noises, vibration of handpieces, and long working hours [Jacobsen and Pettersen, 1993;Jacobsen et al, 1996].…”

Exposure Assessment in Nail Salons: An Indoor Air Approach

“…John et al found that manicurists and nail sculptors were at increased risk of spontaneous abortion [10]. Health effects have been well documented in other workers, such as dental technicians, who work with one of the principal chemicals used in nail salons: ethyl methacrylate [11][12][13][14].…”

Occupational Allergic Contact Dermatitis and Asthma due to a Single Low Molecular Weight Agent

“…In our 3 case reports, the observation of delayed bronchial responses with positive patch tests to LMW agents such as DGEBA or HEMA suggest that expiratory troubles could be linked to a cell-mediated mechanism 16) . The absence of specific IgE to acrylates, methacrylates or human conjugated acrylate-albumin in the individuals with ACD and OA 31) , the absence of positive prick tests to the same conjugated substances 31,32) , and the inconstant presence of specific IgE in asthma to epoxy components 16,17) do not suggest an IgE mechanism. Nevertheless, the absence of specific IgE or positive prick tests to a specific agent often occurs in immediate type hypersensitivity and does not indicate a mechanism of delayed type hypersensitivity.…”