One hundred years of allergic contact dermatitis due to oxidized terpenes: What we can learn from old research on turpentine allergy.

Although in recent years the focus on sensitizing terpene oxidation products has been on oxidized limonene and linalool, the autoxidation of terpenes in relation to allergic contact dermatitis is not new and dates back to the early part of the 20th century with the use of turpentine causing occupational contact dermatitis in painters. This review is written in a way as to allow us to get closer to the work of the scientists in earlier days, to participate in the successes, and also to observe the weak points. The researchers concluded that the main culprit in Scandinavian turpentine was Δ3 -carene hydroperoxides. This explains its high sensitizing effect compared with French turpentine which is of the Iberian type with no or only traces of Δ3 -carene. Historical exposure to turpentine showed that ending the industrial exposure stopped the occupational skin sensitization. Patch test studies demonstrated that monoterpene hydroperoxides, far from being an obsolete source of contact allergy solely related to turpentine, is a common cause of contact allergy in the population. A hundred years of extensive chemical and clinical studies worldwide should be sufficient to meet the evidence requirement regarding allergic contact dermatitis caused by terpenes.

Toxicological Responses of α-Pinene-Derived Secondary Organic Aerosol and Its Molecular Tracers in Human Lung Cell Lines.

Secondary organic aerosol (SOA) is a major component of airborne fine particulate matter (PM2.5) that contributes to adverse human health effects upon inhalation. Atmospheric ozonolysis of α-pinene, an abundantly emitted monoterpene from terrestrial vegetation, leads to significant global SOA formation; however, its impact on pulmonary pathophysiology remains uncertain. In this study, we quantified an increasing concentration response of three well-established α-pinene SOA tracers (pinic, pinonic, and 3-methyl-1,2,3-butanetricarboxylic acids) and a full mixture of α-pinene SOA in A549 (alveolar epithelial carcinoma) and BEAS-2B (bronchial epithelial normal) lung cell lines. The three aforementioned tracers contributed ∼57% of the α-pinene SOA mass under our experimental conditions. Cellular proliferation, cell viability, and oxidative stress were assessed as toxicological end points. The three α-pinene SOA molecular tracers had insignificant responses in both cell types when compared with the α-pinene SOA (up to 200 µg mL-1). BEAS-2B cells exposed to 200 µg mL-1 of α-pinene SOA decreased cellular proliferation to ∼70% and 44% at 24- and 48-h post exposure, respectively; no changes in A549 cells were observed. The inhibitory concentration-50 (IC50) in BEAS-2B cells was found to be 912 and 230 µg mL-1 at 24 and 48 h, respectively. An approximate 4-fold increase in cellular oxidative stress was observed in BEAS-2B cells when compared with untreated cells, suggesting that reactive oxygen species (ROS) buildup resulted in the downstream cytotoxicity following 24 h of exposure to α-pinene SOA. Organic hydroperoxides that were identified in the α-pinene SOA samples likely contributed to the ROS and cytotoxicity. This study identifies the potential components of α-pinene SOA that likely modulate the oxidative stress response within lung cells and highlights the need to carry out chronic exposure studies on α-pinene SOA to elucidate its long-term inhalation exposure effects.